Neurology Flashcards
What is Glia?
Supportive cells throughout the CNS and PNS supporting Neurones, each with different functions.
What are astrocytes?
Glia cells that connect neurones and blood capillaries to form the BBB
What are Satellite cells?
Located in the PNS provide neuronal support
What are microglia?
Immune and Phagocytic functions
What are Ependymal Cells?
They line the CSF filled ventricles and the central canal of the spinal cord
What are oligodendrocytes?
Oligodendrocytes in the CNS provide the Myelin sheath
What are Schwann Cells?
Schwann Cells in the PNS provide the Myelin Sheath
Describe the clinical findings of Relative Afferent Pupillary Defect.
Pupiliary defect:
Light shone on unaffected eye causes full and symmetrical constriction of both eyes, when light swings to AFFECTED eye, the constriction is still symmetrical but REDUCED.
Caused by:
Damage between the Retinal Ganglion and Lateral Geniculate Body.
What is the Lateral Geniculate body?
Located in the Thalamus, it provides a relay station for all the axons of the retinal ganglion cells where the neurons from the lateral geniculate body project, by way of the optic radiations, the occipital lobe, which is the primary cortical area for vision.
What can Relative Afferent Pupillary Defect indicate?
-optic neuropathy
-optic neuritis
-optic nerve compression (orbital tumours or dysthyroid eye disease) –trauma
-asymmetric glaucoma.
What is Miosis?
Pupiliary Defect:
Excessive Constriction of pupil
Causes:Commonly associated with HORNER’s SYNDROME due to a LESION of the sympathetic chain between the hypothalamus and eye.
What can Miosis indicate?
HORNER’s SYNDROME due to …
-Pancoast tumour (lung cancer)
-Trauma
-Thoracic Aortic Aneurysm
How would you confirm Horner’s Syndrome?
4% cocaine eye drops will dilate the unaffected eye BUT NOT the AFFECTED eye.
What is Fixed Dilated Pupil?
Pupiliary defect:
Permanent dilation of pupil that does not constrict on light impulse.
Causes:
Due to sphincter pupillae damage
A patient has Fixed Dilated Pupil. What needs to be excluded?
Third Nerve Palsy
What are the causes of Fixed Dilated Pupil?
-THIRD NERVE PALSY!
-Surgical mistake
-Physical trauma
-Tumour
-Posterior Artery Aneurysm
-Uncal Herniation
A patient has unilateral enlarged pupil / fixed dilated pupil. What could this be due to and how is this medical complaint considered?
Uncal Herniation
=Neurosurgery Emergency
What is Uncal Herniation?
Uncal herniation occurs when rising intracranial pressure causes portions of the brain to move from one intracranial compartment to another. This is usually caused by something increasing the pressure e.g Bleeding in the brain or Tumour
What is Horner’s Syndrome?
Due to a disruption in the sympathetic nerve supply presenting with these triad symptoms :
1.Partial ptosis (drooping or falling of upper eyelid)
2.Miosis (constricted pupil)
3.Facial anhidrosis (loss of sweating)
What are the causes of Horner’s Syndrome?
Most common: Carotid Artery Dissection
(Disruption to the Sympathetic Chain)
Blockage or damage to the sympathetic nerves that lead to your eyes.
The underlying causes of nerve damage CAN VARY WIDELY, from a middle ear infection to a carotid artery dissection or apical chest tumor.
What is Papilloedema?
An INCREASE OF INTRACRANIAL PRESSURE caused by an accumulation of CSF expanding the ventricles (DUE TO HYPERTENSION USUALLY DUE TO MALIGNANCY) and increasing the overall pressure which affects the optic nerves : and causes the SWELLING of THE OPTIC DISC.
A patient presents with headaches and nausea. Upon Fundoscopy, you see that the Optic disc is swollen. What would you do next and why?
Sounds like PAPILLOEDEMA
=1.CT scan of brain
2.If imaging normal, do Lumbar Puncture as Intracranial Hypertension is suspected
What is Mydriasis?
Excessive dilation of the pupil
What are the clinical signs of Third Nerve Palsy?
(See imaging power point)
1.Myadriasis
2.Ptosis
3.Cycloplegia of affected eye
-Exotropia (eye looking outward)
-Hypotropia (one eye always looking upward)
=Issues with accomodation
Additional associated symptoms:
-Fixed dilated pupil and Horizontal Diplopia
A patient presents with Myadriasis, Ptosis and Cycloplegia of her right eye. What artery could have been responsible for ‘this’ and why?
Presentation = Third Nerve Palsy
=Posterior Communicating Artery (runs close to third nerve so an aneurysm of this artery can cause Third Nerve Palsy.
What is Cycloplegia?
Paralysis of accomodation (because of paralysis in the ciliary muscles which are responsible for accomodation).
What is accomodation of the eye?
The eyes ability to focus on images far away AND up close
=Pupil should constrict when something is close (tip of pen) and dilate when far away. If this doesn’t happen : CYCLOPLEGIA
A patient presents with symptoms indicating Third Nerve Palsy however the MR angiography is normal. What is the next step?
Repeat the MR angiography
=Vasospasms of an aneurysm (constriction of the blood vessel) can give a falsely normal MR so repeat it again.
What nerve does Third Nerve Palsy affect?
Oculomotor
What muscle does the Trochlear Nerve innervate and what are the actions of that muscle?
Superior Oblique Muscle of the eye
=Abducting, Depressing and Internally Rotating the eye
What is the most common cause of 4th Nerve Palsy?
Trauma
-due to its long and slender coarse it is very vulnerable to damage
How does 4th Nerve Palsy present?
(See Imaging Power Point)
-Vertical Diplopia
-Excyclotorsion
Can also have :
torsional diplopia, head tilt, and ipsilateral hypertropia.
What is Vertical Diplopia?
Double Vision
=Vertical meaning that the overlapping image will be on top of the other
What is Horizontal Diplopia?
Double Vision
=Horizontal meaning that the overlapping image will be side by side
What is Excyclotorsion?
Affected eye deviates upward and rotates outward when looking in the opposite direction
e.g affected right eye looking left will look upward and rotate outwards
What is the Bielschowsky test and what result would you expect for a patient with 4th Nerve Palsy?
Check head tilting
=Hyperdeviation head tilt
What are the clinical signs of Sixth Nerve Palsy?
-Esotropia ( either one or both of your eyes pointing inward)
-Horizontal Diplopia (double vision with images side by side)
What are the common causes of 6th Nerve Palsy?
-Microvascular Disease (from Diabetes Mellitus and Hypertension)
-External Compression (from acoustic neuroma and raised intracranial pressure)
What is an Acoustic Neuroma?
Acoustic neuromas, also known as vestibular schwannomas, are noncancerous tumours that grow in the ear, and that can affect hearing and balance.
-Cause is largely unknown but regarded to be due to environmental factors such as radiation
What muscle is innervated by the Abducens Nerve?
The 6th cranial nerve innervates the ABDUCTOR MUSCLE OF THE EYE
A patient has Arcuate Scotoma. What Nerve is affected and what are the 4 potential causes of it?
Optic Nerve (1)
1.Glaucomatous Cupping
2.Vitamin B12 deficiency
3.Trauma
4.Optic Neuritis
A patient has Centrocecal scotoma. What Nerve is affected and what are the 4 potential causes of it?
Optic Nerve (1)
1.Glaucomatous Cupping
2.Vitamin B12 deficiency
3.Trauma
4.Optic Neuritis (due to Multiple Sclerosis)
A patient has complete unilateral loss of visual field. What Nerve is affected and what are the 4 potential causes of it?
Optic Nerve (1)
1.Glaucomatous Cupping
2.Vitamin B12 deficiency
3.Trauma
4.Optic Neuritis
What is a scotoma?
Visual blind spot
What is a Centrocecal scotoma?
Blind spot in the centre of the visual field
A patient has Bilateral Hemianopia. What Nerve is affected and what are the potential causes of it?
BRAIN TUMOURS:
-Pituitary tumour
-Craniopharyngioma (tumour between pit. gland and hypothalamus)
-Meningioma (benign tumour arising from the meningeal layers of brain)
=due to issue where the OPTIC NERVES cross at the Optic Chiasm.
A patient has Contralateral Homonymous Hemianopia. What are the potential causes of it?
Tumour, Multiple Sclerosis (MS)
What does Homonymous eye defect mean?
Same visual field in both eyes
A patient has Contralateral Superior Quadrantanopia.What are the potential causes of it?
-Mass lesion in the temoral lobe
-Stroke
A patient has Homonymous Hemianopia. What is the most likely cause of it?
Stroke
What does Hemianopia mean?
A hemianopia is where there is a loss of one half of your visual field
What characterises Parinaud Syndrome?
-Vertical Gaze palsy (cannot look up or down!)
-Convergence Nystagmus
OR
-Diplopia
What is meant by Convergence Nystagmus?
Quick jerking movements of eyes looking inwards
What causes Parinaud Syndrome?
Pineal Gland tumour compressing the vertical gaze centre.
What are the 3 main reasons for patients presenting with Vertigo?
Benign Paroxysmal Positional Vertigo
Meniere’s Disease
Vestibular Neuronitis
A patient presents with hearing loss and vertigo. What could be the most likely cause?
-Meniere’s Disease
OR
-Labyrinthitis
A patient presents with persistent vertigo. What is the most likely cause?
-Vestibular Neuronitis
-Labyrinthitis
What is an Otolith?
Calcium carbonate stone of the ear
What is the pathophysiology of Benign Paroxysmal Positional Vertigo (BPPV)?
Otoliths (stones) get dislodged in the semi-circular canals which produces the sensation of vertigo.
What is the cause of Benign Paroxysmal Positional Vertigo (BPPV)?
Idiopathic HOWEVER
-Most likely to be due to trauma / head injury when it presents in younger people
Who is most likely to present with Benign Paroxysmal Positional Vertigo (BPPV)?
-Over age 50 years
-WOMEN more affected than men
What other disorders is Benign Paroxysmal Positional Vertigo (BPPV) associated with (i.e can present with)?
-Meniere Disease
-Vestibular Neuronitis
A patient has Benign Paroxysmal Positional Vertigo (BPPV). What would you believe to make their symptoms better or worse?
-Provoked by head movement
-WORSEN: Head tilted / on one side/ when waking in the morning
-RESOLVES: When head is kept straight and still
What 2 symptoms if present with vertigo would rule out Benign Paroxysmal Positional Vertigo (BPPV)?
-Hearing loss
-Tinitus
Describe the onset of symptoms of Benign Paroxysmal Positional Vertigo (BPPV)?
Episodic lasting under a mintue and often resolve temporarily when head is kept still.
What investigation(s) are done for a suspected Benign Paroxysmal Positional Vertigo (BPPV)?
Dix-Hallpike test
=A positive test diagnoses BPPV and no more investigations are required.
HOWEVER - if severe neck issues such as Rheumatoid Arthritis or Cervical Spondylosis etc …Cannot do this test and will need to be referred for ENT specialist.
What is the Dix-Hallpike test?
Manoeuvre :
1.Patient lies on side (ear on bed and other facing ceiling) and looks up
2.Look for Nystagmus (jerking of eye)
=If Nystagmus present this is a POSITIVE test and diagnosed BPPV.
What is the management for Benign Paroxysmal Positional Vertigo (BPPV)?
-Epley Manoeuvre (moving head both sides 45 degrees)
-Brandt-Daroff exercises (lying down and looking to one side with eyes closed and doing it on the other side)
=These should be done until 2 consecutive days without symptoms
What lifestyle advice should be given to a patient with a new diagnosis of Benign Paroxysmal Positional Vertigo (BPPV)?
-Avoid driving
-Avoid any tasks that can be adversely affected by vertigo (e.g painting of ladder - you could fall!!)
What is the pathophysiology of Meniere’s Disease?
Somewhat unknown (interplay between genes and enviroment) cause of the EXTENSIVE EXPANSION of the membranous labyrinth which causes the sensation of vertigo.
What is the classical triad of symptoms for Meniere’s Disease?
-Vertigo
-Tinnitus
-Fluctuating Hearing Loss (sensorineural in nature)
What is meant by Aural Fullness?
The feeling of ear pressure or a clogging sensation of the ear
Who is usually affected by Meniere’s Disease?
40-50years
Other than the classical triad of symptoms what other symptoms are associated with Meniere’s Disease?
Aural fullness
Anxiety and Depression
Describe the onset of symptoms in patients with Meniere’s Disease?
ACUTE attack lasting minutes - hours (MOST COMMONLY BEING 2-3HRS)
-These attacks can occur in clusters but often there is a remission period of months before the next one
What investigations are required for a patient with suspected Meniere’s Disease?
NO investigations
-The triad of symptoms ALL being present is enough for diagnosis after REFERAL TO AN ENT SPECIALIST
A patient has been diagnosed with Meniere’s Disease? What advice and legal action is required from you as a doctor?
-Advise not to drive
=Inform the DVLA
-Advise not to perform work that could be adversely affected
What is the management of Meniere’s Disease?
1.Betahistine (to reduce frequency of attacks) to be tried
2.If SEVERE: Admission for IV Labyrinthine Sedatives
3.Prochlorperazine = for use during ACUTE ATTACKS
What are the contraindications for Betahistine?
-Phaeochromocytoma (adrenaline secreting tumour)
-TRY to avoid during Pregnancy and Breastfeeding
A patient is being considered to be put on Betahistine. What should be considered and therefore increase monitoring of the patient’s tolerance of the medication?
Asthma
History of peptic ulcer
Allergic dermatitis
Vomiting
List 3 common side effects of Betahistine.
Gastrointestinal discomfort
headache
nausea
What is Labyrinthitis?
Inflammation of the inner ear
(can also be referred to as Vestibular Neuronitis)
What causes Labyrinthitis?
Inflammation due to a viral (usually being an upper respiratory infection) or bacterial infection.
What are the viral pathogens that can cause Labyrinthitis?
-Varicella-Zoster Virus
-Cytomegalovirus
-Measles
-Mumpes
-Rubella
What are the bacterial pathogens that can cause Labyrinthitis?
Otitis Media
Cholesteatomas
Complication of late-stage syphillis
What is the most common cause of Labyrinthitis in those 30-60years?
Viral
What is the presentation of Labyrinthitis?
-Sudden onset of vertigo associated with nausea and vomiting (can persist up to 72hrs)
-Ongoing Sensorineural hearing loss
-Ongoing tinnitus
What are the main presenting differentiators between Meniere’s Disease and Labyrinthitis?
-Meniere’s usually can be associated with AURUL FULLNESS while Labyrinthitis is not usually associated with it
-Meniere’s mostly presents with the MAIN SYMPTOM being the Vertigo while Labyrinthitis presents with Hearing loss / Tinnitus as the main symptom
What investigations are required for Labyrinthitis?
-Physical exam (Weber and Rinne tests
What type of medication is Prochlorperazine?
Antipsychotic that can also be used to treat severe nausea
What is the management for Labyrinthitis?
For 3 days only (as correcting for too long can affect the body’s compensatory mechanism and therefore disrupt recovery)
-Antihistamines (e.g Cinnarizine)
-Prochlorperazine (anti psychotic)
What does the term palsy mean?
Paralysis accompanied with involuntary tremors
Who is more likely to present with Bell’s Palsy?
Pregnant Women
Describe the presentation of the facial palsy of Bell’s Palsy.
UNILATERAL Palsy (one side of face)
SUDDEN onset
What are the contraindications of Prochlorperazine?
-Avoid oral route in child under 10 kg –CNS depression (substance overdoses, poisoning)
-Comatose states
-Phaeochromocytoma (adrenaline secreting tumour)
A patient is being considered for being put on Prochlorperazine. What underlying health condition should make you monitor them to ensure it is being tolerated?
HyPOthyroidism
When prescribing Prochlorperazine for the elderly, what illness could it potentially worsen?
Parkinsonism or Lewy Body Disease
A patient presents with a facial palsy that is recurrent and bilateral. What differential diagnoses would you consider?
-Sarcoidosis
-Lyme Disease
-Guillain Barre syndrome
-HIV
What is Bell sign?
When the eye rolls when the patient attempts to close it
What is the presentation of a patient with Bell’s Palsy?
-Sudden onset
-Unilateral facial weakness
-Ear ache / preauricular pain
-Eye dryness
-Inability to close eyes fully
-Bell sign (eye rolls when patient tries to close it)
-Hyperacusis (reduced tolerance to sound)
What is Hyperacusis?
Reduced tolerance to sound
-Normal level sounds sound VERY loud
-Loud sounds cause discomfort or pain
How would you differentiate between Bell’s Palsy and stroke based on presentation?
Stroke is an Upper Motor Lesion (Upper spares upper) while Bell’s is Lower.
= Stoke : Can wiggle forehead
=Bell’s palsy : Frozen forehead
What is the prognosis for Bell’s Palsy?
Recovery in 6-9mnths
(only a small number of people are left with permanent effects)
What is the general management for Bell’s Palsy?
-Prednisolone for 10 days
-Eye drops
What is the presentational difference between Ramsay Hunt Syndrome and Bell’s Syndrome?
Ramsay Hunt as well as unilateral facial palsy would also cause PAIN of the face while Bell’s doesn’t
What is the most common cause of Ramsay Hunt Syndrome?
Herpes Zoster Virus
What is usually prescribed to treat Herpes Zoster Virus?
Aciclovir
What is the treatment for Ramsay Hunt Syndrome?
Aciclovir (for the virus) and Steroids
What is the prognosis for Ramsay Hunt?
Less likely (than Bell’s Palsy) to fully recover
How is Postural Hypotension diagnosed?
If there is a change greater than 20/10 on lying / standing BP after standing for 3minutes
A patient on the ward has fainted. What should immediately be done?
Increase salt and water intake
What is cardiac syncope?
A transient loss of consciousness as a result of inadequate cardiac output leading to cerebral hypoperfusion.
What are the causes of cardiac syncope?
-Bradycardia / Tachycardia
-Pacemaker ICD malfunctions
-Structural abnormalities (check with Echo)
-
Who are at an increased risk of epilepsy?
-Family history
-Learning disabilities
-Previous neurological infections
What are the 2 definitions for Status Epilepticus?
-Continuous seizure for 30minutes or longer
-Recurrent seizures without regaining consciousness lasting 30 minutes or longer
What are the 6 groups of seizures?
-Simple Focal (Partial)
-Complex Focal (Partial)
-Secondary Generalised (Focal (partial) progressing to generalised tonic-clonic seizures)
-Absence seizures
-Myoclonic seizures
-Tonic Clonic (grand-mal) seizures
What does simple and complex refer to in terms of seizures?
Simple : Maintaining consciousness
Complex: Impaired consciousness
A pregnant patient has been diagnosed with Epilepsy. What is the treatment?
Lamotrigine
What is Todd Paresis?
Focal weakness of a body part (one side) after a seizure (usually upper or lower limbs).
=This is most likely associated with Epilepsy
Named after the dude who discovered it and also created Hot Toddy’s!
Describe the presentation of simple focal seizures.
-Consciousness retained
-focal motor usual symptoms (muscle jerking)
-can get sensory (tasting/smelling things not there during seizure)
What part of the brain is most commonly affected in a Simple Focal Seizure?
Temporal lobe
Describe the presentation of complex focal seizures.
-May have preceeding aura:
(Unexpected tastes,smells, parasthesia (numbness / tingling) or rising abdominal sensation
-Lip smacking and chewing
-Unable to recall that they just had a seizure
Describe the presentation of Secondary Generalised seizures.
-UNIlateral jerks
-UNIlateral head turning
-Todd Paresis
Describe the presentation of Absence seizures.
-BEGINS IN CHILDHOOD
-Sharp onset and offset - lasting no longer than 30seconds
-Child just stares for a few seconds
-Eyelid Twitching
-May occur dozens - hundreds of times daily
Describe the presentation of Myoclonic seizures.
-Brief shock-like contraction of the limbs
-Conscious attained
Describe the presentation of Tonic-Clonic seizures.
-Stiffening
-Rhythmic limb jerking
-Associated with TONGUE BITING, INCONTINENCE, LOSS OF CONSCIOUSNESS
What investigations are to be done for a pateint after a seizure?
-Bloods (incl LFT)
-U&Es
EEG AFTER 2nd seizure
-MRI (IF FOCAL ONSET)
What characteristics of a seizure suggest a focal origin?
smacking your lips.
rubbing your hands.
making random noises.
moving your arms around.
picking at clothes or fiddling with objects.
chewing or swallowing.
What is considered first line for Focal Seizures?
Lamotrigine or Levetiracetam
(=Broad-spectrum anti-epileptics)
What is the drug of choice for Absence seizures?
Ethosuximide
Carbamazepine is sometimes prescribed for focal seizures. What type of seizure can it worsen?
May worsen myoclonic seizures.
When is Carbamazepine indicated?
Focal seizure, Diabetic Neuropathy
What are common side effects of Levetiracetam?
Mood disorders, Anxiety, and Suicidal ideation
Name 2 examples of Narrow Spectrum Epileptic medications.
Carbamazepine
Phenytoin
Name 4 Broad spectrum anti-epileptic medications.
Levetiracetam
Lamotrigine
Sodium Valporate
Topiramate
What is the main difference between Narrow and Broad spectrum anti-epileptics?
Narrow is mainly for focal while Broad can be used for a wider range (e.g incl Myoclonic)
What is the difference between a primary and secondary headache?
Primary is not associated with anything else while secondary has an attributable cause.
A patient has a headache after intercourse / exertion. What should be excluded first and what is it most likely to be?
RED FLAG: Subarachnoid Haemorrhage
Most likely: Primary Post-Coital or Exertional Headache
What are the 3 main types of Primary Headaches?
-Tension-type headaches
-Cluster headaches
-Migraine
What are the 7 causes of Secondary Headaches?
-Trauma
-Vascular event
-Infection
-Raised intracranial pressure
-Space-occupying lesion
-Disorders that can worsen primary headache
-Medication overuse
What drugs are common causers of Medication overuse headaches?
-Triptans (for cluster headaches)
-Opioids
-Ergots (for throbbing headaches)
-Combination analgesic medication (e.g Co-codamol)
-Paracetamol
-NSAIDs
-Aspirin
What is the definition of a migraine?
Episodic primary headache that CAN present with aura or prove to be chronic.
Who is most likely to suffer Migraines?
Women (3x more likely than men)
What is the pathophysiology of migraines?
Inflammation of Trigeminal sensory neurones causing increased vascular permeability and platelet activation which increases their SENSITIVITY and interpret normal arterial blood flow through the meningeal arteries as PAINFUL
What is the diagnostic criteria for a Migrain WITHOUT aura?
Presentation of 3 or more of these symptoms: POUND
Pulsatile nature
One day’s duration
Unilateral (mainly)
Nausea or vomiting
Disability
What is the presentation for a Migraine WITH aura?
Headache with
-TRANSIENT HEMIANOPIC DISTURBANCES (loss of vision field)
-SPREADING SCINTILLATING SCOTOMA (blind spot)
Aura may include:
-Paraesthesisa
-Numbness of hand, face, upper lips
What mediation in particular would you want to ask a women is on if she presents with Migraine?
Combined Oral Contraceptive Pill.
This contraception is CONTRAINDICATED in women with Migraines WITH Aura
What is the management for a migraine (with/without aura).
-Oral Triptan and NSAIDs (/paracetamol)
Note: Naming for Triptans ends in -triptan
+IF attacks happen >2/month
=Propanolol or Topiramate
A pregnant women has migraines 3 times a month. What medication CANNOT be given to her and what can be given?
CANNOT: Topiramate (Teratogenic!)
CAN: Propanolol
A pregnant patient with Bradycardia has migraines more than twice a month. What would be prescribed as Prophylaxis to prevent migraines?
-Acupuncture
What supplements may reduce the frequency of Migraines?
Riboflavin and Magnesium
A patient describes a ‘tight band’ around head when stressed. What is this?
Tension headache
A patient has chronic recurrent Tension headaches. What would you prescribe?
Tricyclic antidepressants:
Amitriptyline
(titrate down over time)
Describe a cluster headache.
Intense pain coming from within / behind eye
Presents with:
-red watery eye
-nasal congestion
-headache
Who is most likely to have a Cluster Headache?
Men
What is the duration of onset and when do Cluster Headaches classically happen?
-Occur frequently at night
-Can last up to 3hrs!!
What 2 lifestyle factors are linked to Cluster headaches?
smoking and alcohol
What is treatment for an acute attack of a cluster headache?
-100% Oxygen
-Subcutaneous / Nasal Triptan (e.g Sumatriptan)
What are the 2 differentials for Cluster headaches and how do you differentiate them?
1.Chronic Paroxysmal Hemicranias
=Responsive to indomethacin (while Cluster headaches WONT)
2.Short Lasting Unilateral Neuralgiform
=Occur up to HUNDREDS OF TIMES in 24hrs
What is the prophylaxis treatment for cluster headaches?
Verapamil (Calcium Channel Blocker)
What are the main contraindications for Verapamil (calcium channel blocker)?
-Acute Porphyrias (can exacerbate and cause Porphyrias Crisis)
Think: Heart pumping
-Atrial Fibrillation
-Wolf-Parkinson’s-White Syndrome
-Impaired Left ventricular syndrome
-AV block
-Hypotension
-Elderly with postural hypotension (increases risk of falls)
Who is most likely to present with Trigeminal Neuralgia?
-Young patients with MS
-Older patients
Describe the typical presentation of Trigeminal Neuralgia.
Pain in Trigeminal area (jaw area)
=DISABLING CONDITION
-SUDDEN
-Painful, sharp stabbing pain
Note: COMMONLY BILATERAL
What are the secondary causes of Trigeminal Neuralgia?
-Compression from vein or artery
-Arteriovenous Malformation
-Compression from tumour
How is Trigeminal Neuralgia diagnosed?
MRI (to exclude secondary causes)
What is the first line treatment for Trigeminal Neuralgia?
Carbamazepine
What are the common side effects of Carbamazepine?
Dizziness
Drowsiness
Small risk of : Agranulocytosis
What is the next management step for a patients with Trigeminal Neuralgia who is not responsive to Cabamazepine treatment?
-Percutaneous Radiofrequence Coagulation
-Microvascular Decompression /Rhizotomy
=dampen pain signals
What are the common side effects of Calcium Channel blockers?
Abdominal pain; dizziness; drowsiness; flushing; headache; nausea; palpitations; peripheral oedema; skin reactions; tachycardia; vomiting
Name 2 pathological reflexes and would it be upper or lower motor neurone damage?
Upper motor:
Hoffman reflex (upper limbs)
Babinski reflex (lower limbs)
What are the 3 regions of the brain stem?
-Midbrain
-Pons
-Medulla Oblongata
What are gyri and sulci?
Gyri = ridges
Sulci = Depression
What is the Corpus Callosum?
White matter connecting the 2 cerebral hemispheres
What is meant by the cortex in the brain?
The surface of each cerebral hemisphere
What is the Longitudinal Fissue?
=Runs in between the 2 hemispheres
What is the central sulcus?
Located between the frontal and parietal lobes
What is the Pre-Central Gyrus and where is it located?
This is the PRIMARY MOTOR CORTEX
-Located in the frontal lobe towards the parietal lobe
What is the Post-Central Gyrus and where is it located?
This is the PRIMARY SENSORY CORTEX
-Located at the front of the parietal lobe towards the frontal lobe
Name the 3 meningeal layers (from the outer layer to the inner layer)
1.Dura Mater
2.Arachnoid Mater
3.Pia Mater
What are the 2 layers of the Dura Mater?
-Outer Periosteal
-Inner Meningeal
What are Dural Partitions and what do they do?
The folds between the Outer Periosteal and Inner Meningeal layers (of the dura mater)
= They restrict rotary displacement of the brain
Name 4 of the Dural Partitions.
-Falx Cerebri
-Tentorium Cerebelli
-Falx Cerebelli
-Diaphragma Sellae
What is the Terpion?
Where all the bones meet and therefore is the most vulnerable part of the skull
What Artery in the brain is most at risk of damage and why?
The Middle Meningeal Artery
=It lies between the Terpion (at risk area) and the Dura Mater
What are Fontanelles?
Soft spots of bone not fused in new borns
When do the Fontanelles fuse?
Anterior = 7-8mnths
Posterior = 2mnths
Where is primary motor control located and what is it responsible for?
Pre-central gyrus of frontal lobe
=voluntary movements (sends signals to muscles)
Where is primary sensory control located and what is it responsible for?
Post-central gyrus of parietal lobe
=processing sensory information from skin to produce sensations related to temperature, pressure and pain
Where is Primary Auditory control located and what is it responsible for?
Temporal lobe
=analysis of auditory information
Where is primary visual area control located and what is it responsible for?
Occipital lobe
=receives and processes visual information
What is Brocca’s Area and where is it located?
Production of speech
=Frontal lobe of left cerebral hemisphere
What is Wernicke’s Area and where is it located?
Language development
=Temporal lobe of left cerebral hemisphere
What does the Forebrain contain?
-Cerebral Hemispheres
-Thalamus
-Hypothalamus
What does the Hindbrain contain?
-Pons
-Medulla Oblongata
-Cerebellum
What communicates with the Thalamus to coordinate movement?
Basal Ganglia
What is the dorsal horn?
The dorsal horn is found at all spinal cord levels and is comprised of sensory nuclei that receive and process incoming somatosensory information. From there, ascending projections emerge to transmit the sensory information to the midbrain and diencephalon.
What is another name for the Dorsal Horn?
Substantia Gelatinosa
What does Ipsilateral mean?
Same side
(i.e opposite of Contralateral)
Where is a lesion of the Dorsal Column Lemniscal Pathway usually located?
Spinal cord
What are 2 common causes of a lesion of the Dorsal Column Lemniscal Pathway?
-B12 Deficiency
-Tabes Dorsalis (complication of syphilis)
How does a lesion of the Dorsal Column Lemniscal Pathway present?
=Ipsilateral loss of :
-Touch
-Vibration
-Proprioception
!Can still perform tasks requiring tactile information due to the few fibres in the Anterolateral system still functioning
At what level do the 1st order neurones of the Dorsal Column Lemniscal Pathway start?
T6
Where in the spinal cord do the 1st order neurones of the Dorsal Column Lemniscal Pathway travel?
Dorsal Columns
Where in the brainstem would neurones from the Dorsal Column Lemniscal Pathway travel?
Medial Lemniscus
Summarise the Dorsal Column Lemniscal Pathway.
=carries FINE TOUCH SIGNALS FROM PNS TO CNS
1.1st order neurons enter spinal cord at T6 and synapse in the Medulla Oblongata
2.2nd order neurones start in MO and synapse in Thalamus
3.3rd order neurons start in the Thalamus and synapse in the Ipsilateral Primary Cortex of the brain
How does injury to the Anterolateral System present?
=Contralateral loss of pain and temperature sensation
Summarise the Anterolateral system pathway.
=carries Touch & Pressure (anterior) and Pain & Temperature (lateral)
1.1st order neurones enter spinal cord and ascend 2 vertebral levels before synapsing at the Dorsal Horn
2.2nd order neurons split into 2 concurrent tracts (anterior and lateral) that travel to the Thalamus
3.3rd order neurones start in the Thalamus and synapse in the Ipsilateral Primary Sensory Cortex
When are the Spinocerebellar tracts most likely to be damaged?
WITH a Descending Motor injury
(not usually occurring in isolation)
Where in the primary sensory centre in the cortex of the brain is the information processed?
Sensory homunculus
What is another name for pain?
Nociception
When pain presents as fast and sharp, what kind of pain could it be?
Mechanical and Thermal
When pain presents as slow and dull what type of pain could it be?
All types- Chemical, Mechanical and Thermal
Describe the Nociceptor stimulus pathway when due to tissue damage.
Tissue damage causes Calcium to enter which activates TRPV1 Chloride channels = negative ions leaving the cell causes depolarisation which opens enough sodium channels to cause Action Potential.
Describe the Nociceptor stimulus pathway when due to inflammatory signals e.g prostaglandin and bradykinin.
Gprotein coupled receptor causes Calcium release from ER causing activation of Cl- ion channels so Cl- leaves the cell causing depolarisation and therefore Na+ channels on the axons open and cause an Action Potential.
What are the 2 nerves carrying nociceptor signals and speed of conduction as well as the type of pain felt?
Myelinated (rapid signal= fast and sharp) and Unmyelinated neurones (slow signal=slow and dull)
What is another name for Unmyelinated neurones?
C fibres
What is another name for Myelinated neurones?
Alpha delta neurons
Where do the signals usually come from for Myelinated vs Unmyelinated nociceptor neurons?
Myelinated: Skin (superficial)
Unmyelinated : Deep tissue (joints and organs)
Why does pain from Kidney stones present on the same side as the organ and what pain pathway is it?
Gracile Fasciculus pathway (part of the ascending tract) :
Alpha delta fibres (myelinated) carry signals from deep in the body and the information is processed in the thalamus. The fibres DO NOT CROSS OVER and therefore the pain is ipsilateral. Therefore is it hard to pinpoint where the pain is.
A patient has tooth ache. How the pain signalled?
C fibres (unmyelinated) from the trigeminal nerve cross over in the spinal cord into thalamus and into somatosensory cortex to detect exactly where it is
e.g tooth pain
What are the autonomic responses to pain controlled by parasympathetic and sympathetic?
Parasympathetic:
-Bradycardia
-Syncope
-Hypotension
-Urination
-Nausea
Sympathetic:
-Fear
-Pupillary dilation
-Pallor
-Sweating
What is Neuropathic pain?
Pain that is chronic in nature persisting for >3 months and often unresponsive to analgesia.
=Damage to nerves NOT the tissues
How does Neuropathic pain present?
Burning, tickling, dull aches that can be associated with Hyperalgesia or Allodynia.
What is Hyperalgesia?
Increased intensity of pain sensation for a given nociceptive stimulus (that is quite small)
What is Allodynia?
Sensation of pain to stimulus that should not give pain (e.g light touch)
What is meant by sensitisation of peripheral nerves?
Sensitisation of peripheral nerves.
=Increased Prostoglandin release, increases expression of sodium channels and therefore INCREASED NOCICEPTOR SENSITIVITY
What is meant by central sensitisation?
Increased sensitivity of nerves of the spinal cord
1.increased glutamate release and glutamate release causing =Hyperalgesia
2.Rewiring of spinal cord causing
=Allodynia
Describe Descending Pain Pathway in response to pain.
1.Periventricular nuclei in the hypothalamus signals to the 2.Periaqueductal Gray (PAG) which signals via Enkephalin release to the
3.RMN which signals via Serotonin release to the
4.Dorsal Horn inhibitory neurones to inhibit the pain signal via GABA or Enkephalin release
i)GABA
ii)Enkephalin
What does the Descending Pain Pathway do?
Reduces pain signals by decreasing the amount of action potentials and releasing natural opioids.
i.e the body’s natural mechanism to combat pain
Describe the action of Enkephalin released by inhibitory neurons of the Dorsal Horn.
=2 pathways
1.opens Potassium channels to Hyperpolarise and reduce ability to reach Action Potential
2.Inhibits Calcium channels (as it increases neurotransmitters so by inhibiting will mean less signal firing)
Describe the action of GABA released by inhibitory neurons of the Dorsal Horn.
Hyperpolarises by activation of Cl-channels and Cl- enter (so harder to depolarise so less likely to set up action potentials)
How does rubbing a wound help reduce the pain?
Mechanoreceptors signal to brain which descending and deals with the pain (descending pain pathway)
What are the 4 forms of analgesia?
1.Opioids
2.NSAIDs
3.Local Anaesthetics
4.Anti-depressants
Why can Anti-depressants be used to treat pain?
Emotional response to pain makes pain worse.
How do opiods work?
Same as Enkephalin acting on opioid receptors and hyperpolarising the neurons to decrease transmission of signal in the spinal cord
When are opiods used?
For severe pain :
-Surgical pain
-Child birth
-Unresponsive pain
-End of life care (as it has a sedative effect)
Side effects of opiods
Constipation: activates opioids in bowels which opposes gut motility
Vomiting : stimulation of chemoreceptors in medulla
Respiratory depression : Centre in medulla issue, CO2 buildup
What are the withdrawl effects of opioids?
Nausea
Muscle aches
Diarrhoea
Trouble sleeping
Low mood
How do NSAIDs work?
Inhibits COX receptors which inhibits Prostagandin release and therefore causes a decrease in sensitivity
What is the main side effect of NSAIDs?
Blocking Cox receptors protect the stomach as well so NSAIDs can cause GI bleeding, ulcers
When do you give a low vs high dose of aspirin?
High dose for preventing pain
Low dose for issues such as heart attack and stroke
How do Local Anaesthetics work?
Binds and Stops Sodium channels opening so no Action Potentials
How would a Topical local anaesthetic work on an area with a bacterial infection and why?
No effect due to bacterial infection ionising the anaesthetic making it acidic and therefore it cannot reach the sodium channels.
What should be given with a local anaesthetic and why?
Vasoconstrictor such as Adrenaline / Noradrenaline
=keeps the effects of the anaesthetic LOCAL and not widespread
How do Antidepressant work to treat pain?
Increases serotonin which is involved in the descending pain pathway which increasesinhibition of pain signals.
Where does the spinal cord extend to and from?
From the : Foramen Magnum
To the: L1-2 (adults), L3-4 (children)
Where do the nerves leave the spinal cord from?
Vertebral foramens
What is the Cauda Equina?
‘the horse’s tail’ of nerves of the spinal cord after the vertebra
What does the Midbrain contain and therefore is responsible for?
-Eye movement: Nuclei for CN III and IV
-Eye pupil diameter and accomodation: Edinger-Westphal nucleus
-Eye reflexes : Neurons responsible
What is meant by Basal Ganglia?
Interconnecting nuclei within the forebrain, diencephalon and midbrain important for INITIATION AND CONTROL OF VOLUNTARY MOVEMENT including:
-Caudate nucleus
-Subthalamic nucleus
-Substantia Nigra
What is meant by the Limbic system?
Interconnected and interacting structures controlling EMOTIONAL BEHAVIOURS
What is the hippocampus important for?
Memory
What allows storage of new memories ?
Hippocampus has Neurogenesis occuring in the denate gyrus
What is meant by Anterograde amnesia?
Lesion in hippocampus causing memory storage of new memories to not be turned into long memories.
Note: memories from before the lesion are unaffected
What is the Amygdala responsible for?
Emotional learning (fear memory and reward memory e.g addiction)
What neurotransmitter is the most common excitatory in the CNS?
Glutamate
What is the role of the middle ear?
1.Critical Damping = It stops the sound vibrating when the sound stops
2.Amplifies the signal to the oval window
What are the common causative organisms of the meninges?
Remember mnemonic
NHS
-Neisseria meningitidis
-Haemophilus Influenzae (type B)
-Streptococcus pneumoniae
What type of bacteria is Neisseria meningitidis?
Gram negative diplococcus (in pairs)
How is Neisseria meningitidis spread?
Person-person with outbreaks commonly in families, semi-closed environments e.g prisons or university accomodation
What is another name (s) for Neisseria meningitidis?
Meningococcus or Meningococci.
What type of bacteria is Haemophilus Influenzae (type B)?
Gram negative cocco-bacillus
What type of bacteria is the Streptococcus Pneumoniae?
Gram positive diplococcus
What less common bacterial causative organism can cause meningitis and in what groups of people?
Listeria Monocytogenes
=Elderly, Neonates and Immunocompromised persons
What can Listeria Monocytogenes cause?
Meningitis and Sepsis
What type of bacteria is Listeria Monocytogenes?
Gram positive rod shaped
In developing countries what type of meningitis is more likely to occur?
Tuberculosis causing
-associated with miliary TB
How is Listeria transmitted?
Food-bourne
What advice is given to pregnant women to avoid Listeria?
Don’t eat unpasteurised soft cheeses (they could carry Listeria).
What bacteria is tested for in the vagina of a pregnant woman to ensure that it doesn’t cause Meningitis of the baby during child birth?
Streptococcus Agalactiae aka Group B Streptococcus (GBS)
A pregnant patient’s urine sample comes back positive with Group B Streptococcus. What does that mean and what should be done?
Can cause meningitis for baby which can be caught during child birth.
=Prophylactic antibiotics at the time of delivery (Intravenous penicillin G)
What is the most common fungal cause of meningitis?
Cryptococcus Neoformans
Who is more likely to get Cryptococcus Neoformans causing meningitis?
Those immunocompromised:
-HIV/AIDs
-Chemotherapy
How is Cryptococcus Neoformans causing meningitis diagnosed?
-Indian ink staining CSF showing the capsule surrounding the Cryptococcus.
-Culture and antigen detection test of CSF
Who is most likely to suffer from Toxoplasma?
Immunocompromised patients particularly those with HIV with a low CD4 count
How is Toxoplasma transmitted?
Domestic cats in the UK
What can a Ziehl Neelsen stain identify?
Mycobacteria such as TB
What would you notice in a CSF sample with a patient with Bacterial infection of the CNS?
High neutrophils making the CSF look visibly cloudy
What would you notice in a CSF sample with a patient with a Viral infection of the CNS?
High number of T-lymphocytes, and the fluid will look clear.
What is the drug of choice for Meningitis?
Ceftriaxone
A patient has suspect Meningitis but their lab results are pending. What should be done?
EMERGENCY !
Don’t wait- give IV Ceftriaxone
When can Ceftriaxone not be given and what is given instead?
Penicillin allergy
=Chloramphenicol
What is the drug of choice for Meningitis in Neonates?
Cefotaxime as Ceftriaxone can cause Bilirubin accumulation
What is offered to those who were in close contact with a patient with Meningococcal Meningitis?
Prophylaxsis = Ciprofloxacin
Give an example of an organism that can cause Meningitis accompanied with Encephalitis.
Toxoplasma Gondii
Describe the presentation of a patient with Encephalitis.
-Altered consciousness
-Can lead to coma
-Unusual behaviour
-Confusion
-Seizures may be present
-Fever may be present by not accompanied by a significant rise in CRP and WBC
What viruses of the CNS also cause a characteristic vesicular rash?
Herpes Simplex Virus
Varicella zoster virus (chickenpox)
What is the most common cause of Viral Encephalitis in the UK and what is the pathophysiology?
Herpes Simplex latent virus that reactivates in the trigeminal ganglia and causes infection of the temporal lobes
A patient is febrile and has altered consciousness. What is the most likely diagnosis?
Encephalitis
What are the key investigations for Encephalitis?
CT scan or MRI
=indicates raised intracranial pressure (due to inflammation of brain and meninges)
ECG (sometimes used)
Note: CSF lumbar puncture is contraindicated in patients with high Intracranial pressure
Why is lumbar puncture contraindicated in patients with high intracranial pressure?
Coning
=Life threatening due to Sudden drop in pressure when needle draws CSF can draw brainstem structures throughh the foramen magnum
How does Encephalitis appear on an ECG?
Sharp wave potentials
What is the management for Viral Encephalitis?
-IV ACICLOVIR (Antiviral to target Herpes Simplex and Varicella zoster virus) for 3 weeks
Supportive:
-Ventilation
-Fluid management
-Management of seizures if present
-Steroids for reducing swelling
What are the 3 forms of Aciclovir and what are they generally used to treat?
-Oral : Mild infections
-Topical : Herpetic rashes (cold sores)
-IV: Encephalitis
Summarise the mechanism of action of Aciclovir.
It is a viral analogue of Deoxyguanosine that competes to be incorporated into viral DNA and therefore stops the DNA from replicating. It is much more attracted to viral Herpes Simplex DNA polymerase than human DNA polymerase :)
What herpes virus is common in organ transplant patients?
Cytomegalovirus (CMV)
What prophylaxis is given to organ transplant patients to protect against Cytomegalovirus?
Valaciclovir
What are causes of headaches that present with a fever?
-System illness (flu / vaccine)
-Paranasal Sinusitis (upper resp. tract infection / dental pain)
-Meningitis (viral and bacterial)
-Encephalitis
Where are aneurysms most likely to occur?
Where arteries branch
What is the presentation of Meningitis?
PROGRESSIVE headache with fever
Non blanching rash
Neck stiffness
Photophobia
+Lethargy later on
Give 3 examples of Primary headaches.
Tension, Migraines, Cluster headaches
Describe the presentation of Idiopathic Intracranial Pressure.
-Headache:
–>Non-pulsitile, bilateral headache worsening in the morning or after bending forwards and can be associated with morning vomitting
-Visual disturbances (transient visual darkening)
-Bilateral papilloedema (on fundoscopy)
Who is most likely to have Temporal Arteritis?
Older population over 50
What is an Idiopathic stabbing headache?
Most usually benign headache characterised with stabbing like pain
What 2 signs are tested for upon clinical exam of a suspect meningitis?
Kernig’s and Brudzinski’s sign
=lying patient flat and do leg exercises
A patient has been diagnosed with Meningitis. Other than a doctor’s duty of care to the patient what else should be done?
Meningitis long term prophylaxis for close contacts and notify Public Health agency for contact tracing
What serious issue could a Postural headache indicate?
CSF fluid leak
What are Dural Venous Sinuses?
They are spaces / pathways in the brain located between the periosteal and meningeal layers of the dural mater.
Where does the blood flow come from to the Dural Sinuses?
Diploie of the skull, the inner ear and from the CNS.
Where is the Confluence of Sinuses located?
Back of the occipital lobe
Describe the flow of blood starting from the Superior Sagittal Sinuses.
1.Superior Sagittal Sinus to
2.Confluence of Sinuses to
3.Right Transverse Sinus to
4.Right Sigmoid sinus (merging with left SS to become)
5.Internal Jugular Vein
Describe the flow of blood starting from the Inferior Sagittal Sinuses.
1.Inferior Sagittal Sinus to
2.Straight Sinus to
3.Left Transverse Sinus to
4.Left sigmoid sinus (merging with left SS to become)
5.Internal vein
Where are the Right and Left Transverse Sinuses located?
Posterior cranial fossa
Describe the flow of blood from the Cavernous Sinus.
1.Cavernous Sinus to
2.Superior sagittal Sinus
3.Junction between Left transverse and Left Sigmoid sinus
4.Petrosal Sinuses to
5.Internal Jugular vein
Where are the Cavernous Sinuses located?
Just lateral to the sphenoid bone
Where do Cavernous Sinuses receive their tributaries from?
Opthalamic veins
Sphenoparietal sinuses (along the lesser wing of sphenoid bone)
Where is CSF secreted?
By Choroidal Epithelial cells of the choroid plexus in the lateral, 3rd and 4th ventricles
What is meant by the Ventricular System?
The pathway by which CSF flows in the brain
Where is CSF reabsorbed?
Arachnoid Granulations which protrude through the meningeal layer of the Dura Mater to access the Sinuses
Describe the flow of CSF.
1.Lateral Ventricle to
2.Interventricular Foramana to
3.3rd Ventricle to
4.Cerebral Aqueduct to
5.Lateral Apertures to
6.Subarachnoid space to
(some reabsorbed)
7.Median Apertures to
8.Spinal cord (Central Canal)
What would an obstruction of the Cerebral Aqueduct mean?
Blockage of CSF meaning that it can’t leave the Subarachnoid space
=Hydrocephalus
What procedure should be considered for a patient with Hydrocephalus?
Peritoneal Shunt
=drains the CSF into the Peritoneal cavity (abdomen)
Define the Central canal.
Carries the CSF along the spinal cord
What are the key risk factors of a brain haemorrhage due to an aneurysm?
-Smoking
-Hypertension
-Polycystic kidney disease
-Connective tissue disorders (since they affect the integrity of the blood vessels)
What is the investigation for Subarachnoid Haemorrhage (starting with first line)?
1.CT brain AS SOON AS POSSIBLE (as the bleed will disperse and you’ll miss the diagnosis)
2.Lumbar puncture
=look for bilirubin (Xanthochromia - yellow CSF)
3.CT Angiogram (if CT brain is positive to find what artery is responsible)
What blood vessel is most likely to have had an aneurysm to cause a brain haemorrhage?
Right middle cerebral artery
Where do you do a lumbar puncture?
Iliac crest at L4
List the contraindications of doing a lumbar puncture.
-Coagulopathy
-Local infection at puncture site
-Focal neurology and abnormal conscious level
When can you do a lumbar puncture and when is it too late?
Can: Within 2 weeks of a headache
Cannot: After 2 weeks because you won’t be able to detect the bleeding anymore
A patient had a haemorrhage due to an aneurysm. What is the main treatment?
Coiling
When is Vasopasm most likely to happen and why?
During Subarachnoid haemorrhage due to oxygen present since its due to arterial bleeds while a head injury is due to venous bleeds
What is the Vasospasm treatment?
Bolus IV Saline / Colloid
What are complications of a Subarachnoid Haemorrhage?
-Hydrocephalus
-Seizures
-Low sodium
-Pulmonary oedema / pneumonia
What is the prognosis for a Subarchnoid haemorrhage?
Poor- most survivors are dependant with only 20% of survivors regaining full quality of life. Note that 30% don’t even make it to hospital!
What are the causes of Intracerebral Haemorrhage?
-Hypertension
-Vascular Lesions
-Neoplastic
-Coagulation disorders
-Cerebral venous thrombosis
-Haemorrhagic transformation of ischaemic stroke
-Vasculitis
-Substance abuse
-Amyloid
What veins are most likely to be a cause of a haemorrhage in a Hypertensive emergency?
Small vessels deep in the brain (that supply the motor pathways)
What investigations are to be done for a suspect
Idiopathic Intracranial Hypertension and what results would you expect?
-Fundoscopy (bilateral papilloedema)
-CT and MRI of brain (increased intracranial pressure)
-Lumbar puncture (will reveal opening pressure above 20cmH20 but no differences in the CSF profile)
What is the management for Idiopathic Intracranial Hypertension?
1.Encourage weight loss
2.Acetozolamide (Carbonic Anhydrase inhibitor)
3.Topiaramate (anti-seizure med) and Candesartan (ARB)
Who is most likely to present with an Idiopathic Intracranial Hypertension?
Young, obese women
What is Temporal Arteritis?
Inflammatory disease of the arteries specifically the arteries at the temples.
What is another name for Temporal Arteritis?
Giant Cell Arteritis
What is the presentation of Temporal Arteritis?
-Temporal headache
-Pain on temples
-Jaw claudication (pain chewing food)
-Transient monocular blindness
-Systemic features (fever, fatigue, weight loss and malaise)
Who is most likely to be affected by Temporal Arteritis?
Females over 60
What will be found on presentation on a patient with Temporal Arteritis?
-Thickened, tender temporal artery on examination, which may be pulseless
-Scalp tenderness
-(Rarely) arterial bruits, asymmetrical blood pressure and absent pulses
What are the key complications of Temporal Arteritis?
-Permanent monocular blindness
-Stroke
-Aortic aneurysms
How do patients describe Monocular blindness?
Curtains closing on their vision
What investigations are to be done for Temporal Arteritis and results?
1.Inflammatory markers (present)
2.Histology : Granulomatous inflammation with infiltration of inflammatory cells including giant cells
3.Doppler Ultrasonography (halo sign within vessel wall)
What is the management of Temporal Arteritis?
-High dose steroids to prevent blindness and stroke
(titrate down over time with methotrexate to lower the dose)
-Low dose aspirin
If on long term steroids:
+Bisphosphonates (protect against Osteoporosis)
+PPIs (protect against gastric ulcers)
A patient has a new onset headache. What are the categories within this?
-Thunderclap
-Fever
-Focal
-Persisting
-Provoked
What are the differentials of a thunderclap headache?
-Subarachnoid Haemorrhage
-Pituitary Apoplexy
-Spontaneous Intracranial Hypotension
Summarise how you would differentiate between the 3 types of thunderclap headache simply based on symptoms?
Subarachnoid: MOST SEVERE
Pituitary Apoplexy : With drowsiness often progressing to coma
Spontaneous Intracranial Hypotension: Positional headache
How is the diagnosis of a Subarachnoid haemorrhage confirmed?
CT without contrast
-If CT negative Xanthochromia in CSF will confirm it
A patient has a Subarachnoid Haemorrhage. What should be done?
-Angiography with catheter to localise bleed
-Endovascular coiling
-Post op: Nimodipine
What is the management for Pituitary Apoplexy?
Hydrocortisone (GIVEN ASAP AS IT COULD BE FATAL)
-do an mri
What investigation should be done for Spontaneous Intracranial Hypotension?
MRI of whole spine
What is the management of Spontaneous Intracranial Hypotension?
Bed rest fluids, caffeine and pain relief (if it doesn’t improve - Epidural blood patch)
What is the most likely diagnosis of a Fever new onset headache and what is the red flag diagnosis to rule out?
Most likely = Systemic
Red flag: Meningitis
What is meant by a new onset focal headache?
One part of brain being affected can present as MOVEMENT CHANGES, PARALYSIS, WEAKNESS, LOSS OF MUSCLE CONTROL, INCREASED MUSCLE TONE, LOSS OF MUSCLE TONE OR INVOLUNTARY MOVEMENTS (E.G TREMOR)
What are the 2 main possibilities for a focal new onset headache?
-Migraine with aura
-Stroke
How do you differentiate between migraine with aura and stroke upon presentation?
Migraine aura resolves while stroke aura persists
List the Persisting New onset headaches.
-CO poisoning
-Giant Cell Arteritis
-Cervicogenic
-Paranasal sinus
-Tumour
-High CSF pressure
List the provoked new onset headaches?
-Exertional / Coital headache
-Cluster
-Trigeminal neuralgia
What are the possible differentials of recurrent headache?
-Tension
-Ice pick
-Cervicogenic
-Migraine with or without aura
What is the presentation of an Ice Pick Headache?
Sudden episodic sudden, sharp, stabbing head pain (or a quick series of pains)
What is the treatment for Ice pick headaches?
If severe and frequently reoccuring:
Indometacin
What is the presentation of Idiopathic Intracranial Hypertension?
-Changes in vision
-Peripheral vision loss -Neck stiffeness
-Trouble waking
-Vomiting and nausea
What is the treatment for Idiopathic Intracranial Hypertension?
Diuretics
What investigation is done for Idiopathic Intracranial Hypertension?
MRI
What is the first line management for Migraine with or without aura?
-Oral triptan + paracetamol / NSAID
(nasal for ages 12-17)
Prophylaxsis:
-Propranolol or Topiramate
What is the management for Tension-type headaches?
-Paracetamol / NSAIDs (Ibeprofen 400mg)
-Prophylaxsis : Acupuncture
What is the management for Cluster Headaches?
-100% Oxygen
-Subcutaneous / Nasal Triptans
-Prophylaxsis: Verapamil (calcium channel blocker)
A patient with migraines after first line treatment has found no improvement. What is the next management step?
Addition of an Anti-emetic e.g Metoclopramide or Chlorpromazine
What supplements can be suggested for patients with migraines?
-Riboflavin (B2)
-Magnesium
A patient with Tension headaches has found no improvement despite first line treatment. What is the next management step?
Addition of a Tricyclic antidepressant (Amitriptyline)
How do Triptans work?
Serotonin Receptor agonist
Remember: Serotonin release activates inhibitory interneurons in the spinal cord
How do Anti-emetics work?
Block specific receptors that respond to neurotransmitter molecules, such as serotonin, dopamine and histamine.
How do Tricyclic Antidepressants work?
Inhibit reuptake of Serotonin and Norepinephrine to elevate concentration within synaptic cleft which therefore increases blocking of pain
What is meant by the spinal cord level of neural integration?
-Stereotypical behaviours
-Reflexes
What is meant by the subcortical level of neural integration?
Medulla and Pons supervising spinal reflexes
What is meant by the cortical level of neural integration?
Highest level of neural activity
What level of neural integration is affected in Stroke?
Cortical gone, but not subcortical and spinal cord level which is why you would still have spasticity
What neural fibres in the muscles are important for sensing lengthening and stretching of a muscle?
For example : Elongating your arm
Extrafusal fibres made up of muscle spindles called Intrafusal (membrane and nerve to detect stretch and length of a muscle)
What is meant by a muscle spindle?
Collection of nerves (lower motor nerves) in the muscles for detecting movement of muscle (stretch and forceful movement)
What are the 2 types of Intrafusal fibres within the muscle spindle?
Nuclear bag
Nuclear chain
Within the muscle spindle, what are the 3 main sections and what are they composed of and what are they responsible for?
Nuclear Bag =VELOCITY (of moving muscle)
-Type 1Alpha fibres : Fast conducting so stop conducting immediately once the signal has stopped
Nuclear Chain=Stretch / Length (of the muscle being moved)
-Type 2Alpha fibres : Slow conducting so still conducting even when signal has stopped.
Gamma Efferent Fibres = Stop the muscle from become floppy as it sets the baseline tone of muscle
What is the difference of function between Alpha and Gamma muscle spindle neurons?
alpha = voluntary control
gamma = subconscious control setting baseline tone
What are the function of muscle spindles?
=Have alpha and gamma fibres for voluntary and subconscious moving,smoothing and dampaning of muscle contractions (e.g elongating arm) :
E.g of subconscious muscle control:
-deactivate antagonist muscle
-signals length and velocity of muscle stretch to cerebellum (for conscious and unconscious awareness of length of muscle i.e arm elongated)
-i.e proprioceptive understanding of where your arm is
Where is the Golgi tendon organ and when is it activated?
Nerve ending interdigitating with TENDON via Alpha neurons
=do not activate unless there is A LOT of muscle contraction force not passive STRETCH
Compare passive stretch and muscle contraction force
Passive stretch is the conscious (basic movement e.g walking) and subconscious (proprioceptive understanding of where your body parts are), this is controlled by muscle spindles.
While Contraction force is for tasks such as lifting which is controlled by the Golgi Tendon Organ.
What is the function of the Golgi tendon body?
Forcfully control force and length so that you can carry something (e.g a dumbell)
-sensitive to how heavy it is and is therefore responsible for telling you if it is slipping out of your hands as it is too heavy
What do Facial muscle reflexes indicate?
Hypocalcaemia
Describe the pathophysiology of a 8hz physiologic tremor?
The Brain supervises the stretch reflexes so in a stroke for instance , the reflexes are not supervised and therefore HYPER-REFLEXES
=clonus
When would you get pathologic clonus?
Stroke
ALS
MS
UM Lesions
Hepatic Encephalopathy
What is meant by clasp knife rigidity in Upper Motor Lesions?
Initial resistance (passive strength fibres are over signalling position and therefore resistant to move) to elongate arm and then sudden, quick and forceful (golgi tendon overactive giving force) elongation
LIKE A CLASP KNIFE
What is meant by Spastic posture and what tract is responsible?
Upper: Flexed elbows and wrist, Clenched wrist
Lower: Plantar flexed foot and toes
=Pyramidal tracts
Where is the Vestibular Nucleii and what does it do?
Between pons and medulla, position and posture sense that goes down the Vestibulospinal tract
Where is the Vestibulospinal tract (Lateral or Medial)
Medial
What is the Final Common Path?
Descending motor pathway whereby 1 motor neurone recieves input from multiple different descending motor pathways (e.g Rubrospinal and Corticospinal etc)
Where is the location of 60% of intracerebral haemorrhages?
Internal capsule which is involved in the pyramidal descending motor pathway.
What is Babinski sign and what does it mean?
Plantar reflex = Big toe points upwards rather than curl downwards
= UML
Describe the Putamen circuit and what is it’s function?
Motor cortex to putamen in the basal ganglia to Substantia nigra to thalamus back to the motor cortex
=Learning and motor control (e.g speech articulation, cognitive functioning and addiction)
What does Athetosis mean?
Abnormal muscle contraction causing involuntary writhing movements
e.g in Cerebral Palsy
What does Ballismus mean?
Involuntary throwing/flinging movements of limbs caused by large muscle contractions
What does Chorea mean?
Sudden, unintended and uncontrollable jerky movements of arms, legs and facial muscles
e.g huntington’s chorea
Describe the Caudate circuit. What is it responsible for?
From brain, to putamen, globus palludis, thalamus to brain
=Planning movements and cognitive control (desire to move - do i want to get out of bed?)
What is the physical connection between the Substantia Nigra and Striatum?
Excitory connection releasing Dopamine
What causes Parkinson’s?
Degeneration of Dopamine neurones from the Substantia Nigra to the Striatum
=Hyper and Hypokinesia (tremor)
Compare the type of rigidity of Parkinson’s vs of a Stroke.
Parkinson’s: Lead pipe + Cogwheel
Stroke: Clasp knife
What is the function of the Spinocerebellum?
Responsible for matching intended movement (signals from motor cortex) with the actual movement that is done (proprioceptive muscle spindles).
What is the function of Cerebrocerebellum?
Planning movements and ensuring accuracy e.g picking up a pencil
Skills learnt (usually in an adult) are stored here e.g learning to drive, sports, even a new language learnt after age 8 while a first language would be stored in Broca’s area)
What are the presentation hallmarks of a Vestibulo and Spinocerebellar problem?
=wide stance
=swaying while standing
=inappropriate =nystagmus
=ataxic gait
What are the presentation hallmarks of cerebrocerebellar problems?
=movement accuracy =compromised
decomposition of movements (e.g picking up a pencil will take ages as each mirco movement has a pause in between and won’t be smooth)
=intention tremor
Intention tremor vs parkinson’s tremor
Intention: moving from different places when trying to pick up a pencil for instance
Parkinson’s : Pill rolling
What are the 3 parts of the Cerebellum?
Vestibulocerebellum, Spinocerebellum and Cerebrocerebellum
4 lesion locations
UMN
LMN
Extrapyramidal
Cerebellar
What is meant by Anticipatory maintenance of posture?
Other muscles will contract in anticipation of the planned movement to support balance
Define what a Upper and Lower Motor Neuron is?
UMN: Brain or Spinal Cord
LMN: Anterior horn cell, motor nerve roots, peripheral motor nerve
What happens to the stretch reflex in issues with UMN and how does it present?
Exaggerated stretch reflex (due to lack of control and inhibition)
=Spasticity e.g clonus
Spascitisty vs Rigidity
Spasticity = damage to Pyramidal tract:
Increased tone in only part of the movement
Rigidity = damage to Extrapyramidal tract :
Increased tone throughout range of movement
What does Hemiplegia mean vs Hemiparesis?
Hemi: One sided
Plegia: Paralysed
Paresis: Weakness
A patient has a Cervical lesion (up to C5), what is the hallmark presentation?
-Spastic quadraparaesis
=All 4 limb weakness and spastic posture
A patient has Thoraci and lumbar spinal lesion, what is the hallmark presentation?
Spastic paraparesis (impaired not completely lost in lower limbs)
List UMN issues.
-stroke
-brain tumour
-ALS
-intracranial haemorrhage
-post head injury / trauma
-MS
-Spinal cord stenosis
-Prolapsed disc
Upon beside and gait inspection, what would you expect for a LMN?
Fasciculations
Waddling Gait
Describe the hallmark presentation of Guilliene-Barre
flaccid Paraplegia losing reflexes
Proximal vs Distal weakness (LMN)
Distal - Focal or Widespread (e.g Peripheral neuropathy - diabetes)
=difficulty with fine tasks e.g writing
Proximal = Difficult with rising, walking stairs
=Muscular Dystrophy, Rediculopathy
Fatiguable weakness
Ocular and Bulbar e.g Myasthenia Gravis
What is meant by the LMN Foot drop?
Cannot dorsiflex foot, wasting of Tibialis anterior muscle
in nerve = weakness and numbness
What is meant by LMN wrist drop and what are the causes?
wasting of triceps, unable to extend wrist
=radial nerve lesion of the axilla
causes:
-trauma
-humeral fracture
-motor neurone disease
Give examples of LMN.
GP:
-Radiculopathy
-Bells palsy
-Peripheral neuropathy
-Occular Myasthenia Gravis
-Muscular Dystrophy
Hospital:
-Motor neurone disease
-Cauda Equina
-Guillain-Barre
-Myasthenia Gravis
-Inflammatory myopathies
Where is there Dual pathology and give an example.
Anterior horn cells of the spinal cord = where the nerve tracts overlap
=Motor Neuron Disease
What are the hall mark features of Extrapyramidal disease
(Basal Ganglia)?
-no weakness
-disorder of movement:
=sequencing and smooth fluid control
-jerking
-rigid tone
-bradykinesia
-resting tremor
-shuffling gait
=Parkinson’s
What is meant by Sensory Ataxia and what are the causes?
=loss of movement proprioception
e.g when you are drunk with alcohol
-Cerebellar lesion
-Stroke
-MS
-tumour
Do Cerebellar lesions present as contra or ipsilateral?
Ipsilateral
What common drug can cause a tremor?
Salbutamol
Where is the Substantia Nigra?
Midbrain
What is the Striatum?
Largest structure of the Basal Ganglia
How would you differentiate between a UMN lesion in the brain vs in the spinal cord?
Brain:
-Contralateral Hemiplegia
-Flexed Upper limbs
-Extended Lower limbs
Spinal cord:
Quadriplegia (cervical) and Paraplegia (thoracic / lumbar)
What does Paraplegia mean?
Complete paralysis of legs
What does Quadraplegia mean?
Complete paralysis of all 4 limbs
A patient has a Cervical Lesion- how does that affect the limbs?
Quadriplegia
A patient has a Thoracic / Lumbar Lesion- how does that affect the limbs?
Paraplegia
What are the 2 most common causes of UMN issues?
Multiple sclerosis, road traffic accident
Describe the Anterolateral pathway.
This is an Ascending (Somatosensory) Pathway
1.Starting from the Sensory receptors of the Periphery
2.Enters the spinal cord and ascends 1-2 levels
3.Synapse at the Dorsal Horn (Substantia Gelatinosa)
4.Splits into 2 tracts - Anterior and Lateral
5.Travel together and ends in the Thalamus
What is the Anterior Anterolateral tract responsible for?
Touch and Pressure
What is the Lateral Anterolateral Tract responsible for?
Pain and temperature
What syndrome is the most common cause of damage to the Anterolateral System and what would therefore be presented?
Brown-Sequard Syndrome
=Contralateral loss of pain and temperature sensation
What are the Pyramidal pathways?
Descending motor pathway responsible for voluntary motor control of musculature of body and face
What are the Extrapyramidal pathways?
Descending motor pathway responsible for involuntary automatic control of all musculature such as muscle tone, balance, posture and locomotion.
What 2 pathways are part of the Pyramidal pathway system?
Corticospinal and Corticobulbar tracts
What pathways are part of the Extrapyramidal pathway system?
-Vestibulospinal
-Reticulospinal
-Rubrospinal
-Tectospinal tracts
What is the Vestibulospinal tract responsible for?
Ipsilateral Balance and Posture
What is the Reticulospinal tract responsible for?
-Ipsilateral Muscle tone (medial increases and lateral decreases) and Voluntary movements (medial facilitates and lateral inhibits) (ipsilateral)
What is the Rubrospinal tract responsible for?
Contralateral Fine control of hand movements
What is the Tectospinal tract responsible for?
Contralateral Coordination of head in relation to vision stimuli
What is the Cortiocospinal tract responsible for?
Voluntary motor control of musculature of body
What is the Corticobulbar tract responsible for?
Voluntary motor control of musculature of face and neck
Describe the Corticospinal Pathway.
Descending motor pathway
1.Recieves information from the Primary motor cortex, Premotor cortex, Supplementary motor area and Somatosensory area
2.From the Thalamus
3.To the Medulla
4..Motor neuron splits into anterior and lateral
5.Lateral crosses over and the Anterior remains Ipsilateral
6.Ends at the Ventral horn
What is a Capsular Stroke?
The internal capsule (between the thalamus and basal ganglia) is extremely susceptible to compression from HAEMORRHAGIC BLEEDS
=causes a lesion of the descending tract
Describe the Corticobulbar tract.
1.From the Lateral aspect of the primary motor cortex
2.Through Internal capsul to midbrain, pons and medulla oblongata
3.Lower motor neurones innervate the face and neck
4.Innervates cranial nerves
What are somatic senses?
Temperature
Touch
pressure
vibration
proprioception
pain
What are nociceptors?
Mechano-thermo and chemothermoreceptors resulting in PAIN
What makes the finger tips increased sensitivity compared with your back?
The receptive fields (the areas that sense stimulus) overlap while the receptive fields on the back are further apart and therefore not as sensitive.
What is meant by a Phasic response?
Transient response with a quick Action potential that resolves quickly e.g pain
What is meant by Tonic response?
The excitability of the neuron is maintained giving constant sensation e.g Proprioception.
List the types of Mechanoreceptors.
-Tactile receptors (majority on skin and some in deep tissue)
-Proprioceptors (e.g Muscle spindles, Golgi tendon etc)
-Baroreceptors (Cardiovascular)
-Inner ear receptors (cochlear and vestibular)
What are TRP channels?
Protein channel recptors situated in the skin, hypothalamus, skeletal muscle, spine and liver that open for different temperature ranges.
e.g
-Menthol (mint) is an agonist for TRPA1 which activates this protein channel creating a cool sensation
-Chilli is an agonist for TRVP1 which activates the protein channel receptor and creates a hot sensation
What is meant by the Spinal Lamina?
In the ascending tract, the C fibres (pain + temperature) do not infiltrate very far into the grey matter while Alpha fibres (proprioception) infiltrate a lot deeper into the ventral horn meaning that there are LAYERS IN THE BRAIN THAT PROCESS DIFFERENT TYPES OF INFORMATION FROM THE DIFFERENT TYPES OF NEURONAL FIBRES.
Give an example of a dermatomal illness and its basic pathophysiology.
The infection (e.g Shingles) lies dormant in the Dorsal root ganglion of the sensory nerves and (if immunocompromised) will travel down nerve and express at the dermatome.
Where do the cell bodies of sensory neurons lie?
Dorsal Root Ganglia (DRG)
What is the most common cause of Meningitis?
Viral (Coxsackie virus)
Note: Bacterial incidences have significantly decreased with the vaccine.
What is Mollaret Meningitis?
A form of aseptic meningitis characterised by recurrent episodes of meningism interspersed with symptom free weeks (associated with Herpes Simplex 2)
What are the key investigations for a suspect case of Meningitis and would you expect the results to be?
!Provide empirical antibiotics IMMEDIATELY rather than wait for investigation results to come back
1.Lumbar puncture (Raised Intracranial pressure, fluid clear with elevated glucose, protein)
2.Bloods (Viral PCR, ABG, CRP, U&E etc)
What is the management for Meningitis?
1.IV Ceftriaxone / Cefotaxime for 10 days
If a patient is <3months or >50 years, what should be added to their management plan for Meningitis?
-Add Amoxicillin IV for 14 days
(Or Chloramphenicol if allergic to Penicillin)
A neonate / infant has meningitis. What can’t be given as part of their management and why?
Ceftriaxone causes worsening of jaundice and acidosis
-Give Cefotaxime instead
If Viral Meningitis or Encephalitis is suspected, what should be given?
IV Acyclovir
What is the presentation of Encephalitis?
Classic triad of rapidly progressing symptoms:
-Fever
-Headache
-Altered mental status
What is the pathophysiology of Encephalitis?
Inflammation of the parenchyma due to viruses most frequently:
-Herpes Simplex 1 = Herpes Simplex Encephalitis affecting the temporal lobes
What other viral infection can Encephalitis occur with?
Meningitis
Who is most likely to suffer from Encephalitis?
Neonates, elderly and immunocompromised
What investigations are to be done for a suspect Encephalitis patient?
-Lumbar puncture
-Blood tests
-Neuroimaging (CT/MRI)
What would a ring enhancing lesion on a CT/MRI indicate and what should be initially done?
-Cerebral Abscess
-Tumour
-Metastasis
-Demyelination
=Neurosurgical referral
A patient has a cerebral abscess. What should be administered?
IV Ceftriaxone
What is the management for Encephalitis?
-Prompt IV Acyclovir
-Empirical antibiotics
-Monitoring for seizures
What should NOT be done with a patient with Encephalitis?
-Corticosteroid administration
-Excessive fluid therapy (can exacerbate cerebral oedema)
List the risk factors for developing a stroke.
-Hypertension
-Smoking
-Diabetes Mellitus
-Hypercoagulability
-Hyperlipidaemia
-Combined Oral Contraceptive Pill
-Trauma
-Atrial Fibrillation!
-Anticoagulation (due to increased risk of bleeds)
What are the 4 classifications of a stroke that would be assessed in A&E?
1.Total Anterior Circulation Infarct
2.Partial Anterior Circulation Infarct
3.Lacunar Infarct
4.Posterior circulation Infarct
What are the 2 types of stroke?
Ischaemic and Haemorrhagic
What is meant by a Total Anterior Circulation Infarct?
Large infarct of the main stem of the Middle Cerebral Artery or Anterior cerebral artery
!WORST PROGNOSIS- LIFE THREATENING!
What is meant by Partial Anterior circulation infarct?
Branch of Middle Cerebral artery / anterior cerebral artery infarct
What is meant by a Lacunar stroke?
Occlusion of the small arteries around the thalamus, pons, basal ganglia and internal capsule
What is meant by a Posterior Circulation Stroke?
Vertebasilar stroke affecting the cerebellum / brainstem
What is the presentation of a stroke due to the Anterior Cerebral Artery occlusion?
-CONTRAlateral sensory and motor weakness
-LOWER LIMBS symptoms are more dominant
What is the presentation of a stroke due to the Middle Cerebral Artery occlusion?
-CONTRAlateral sensory and motor weakness
-UPPER LIMBS symptoms are more dominant
-CONTRAlateral homonymous hemianopia
-Aphasia
What is the presentation of a stroke due to the Posterior Cerebral Artery occlusion?
-CONTRAlateral homonymous hemianopia
-Macular sparing
What does Macular sparing mean?
Visual defect where only the central visual field can be see
What is the presentation of a stroke due to the Anterior Cerebral Vertebasilar Artery occlusion?
-Loss of Consciousness
-Homonymous Hemianopia occuring in ISOLATION
A patient has a suspect stroke. What are the investigations to be done?
URGENT: CT/MRI (CT usually preferred)
=Exclude Haemorrhagic stroke
-Assess for hypertension
-Bloods and U&E
-Speech and language assessment
-ECG (AF?)
-Echo (Embolism or Vascular disease?)
-Carotid Artery duplex ultrasound
What is the initial management for an Ischaemic stroke?
1.Alteplase (thrombolysis)
-If swallow impaired
2.=NG tube
3.Aspirin (300mg) orally or rectally if swallowing impaired
A patient has a stroke due to their hypertension - what procedure should therefore be considered?
Carotid Endarterectomy (for treating stenosis)
What is Aspiration pneumonia, and what type of patients are most at risk of it?
Serious complication associated with stroke presenting as chest pain with coughing up of green sputum with pus or blood as well as wheezing. Therefore swallowing should always be assessed.
Describe the post-stroke treatment plan?
1.Aspirin for 2 weeks
2.Switch to oral Clopidogrel 75mg once daily
IF ATRIAL FIBRILLATION
+Anticoagulation
IF HYPERTENSIVE
+Statin
What is the definition of a Transient Ischaemia Attack?
Acute cerebrovascular pathology that resolves within 24hrs
How may a haemorrhagic stroke present differently than a ischaemic stroke?
Similar focal symptoms BUT
-Pronounced headaches
-Neck pain
-Photophobia
-Nausea and Vomiting
What is the ABCD2 score for a patient that has had a TIA?
A score of more than or equal to 4 suggests a high likelihood of a stroke in the future:
Age : >60yrs = 1 point
Blood pressure >140/90 = 1 point
Clinical features
-Unilateral weakness = 2 points
-Slurred speech, absence of motor weakness = 1 point
Duration of symptoms
>1hr = 2 points
10-59mins = 1 point
Diabetes Mellitus = 1 point
If a TIA patient has an ABCD2 score of >/= to 4, what is the management?
300mg Aspirin daily
Specialist assessment and investigation within 24hrs
If a TIA patient has an ABCD2 score of <4, what is the management?
300mg aspirin daily
Specialist investigation and assessment no later than 1 week
What is meant by Crescendo TIA?
A patient presenting with 2 or more TIAs within a week (puts them at high risk of stroke despite their ABCD2 score).
What is Amaurosis Fugax?
Means fleeting darkness and is a visual field defect described as “a curtain coming down on their vision”.
=Caused by emboli from the ipsilateral carotid artery representing a nonhemispheric TIA (could be cerebellar / brain stem).
A patient had Amaurosis Fugax, what investigative step should be done?
=Curtains coming down on vision
–>Carotid artery imaging
Compare Focal vs Diffuse brain injury.
Damage to one part of the brain (e.g impact to the head) vs injury across the whole brain (e. road traffic incident whereby the brain is bashed within the skull and therefore the damage is widespread).
What is meant by Diffuse axonal injury?
Tearing of the nerves throughout the brain - type of traumatic head injury
What is meant by Diffuse vascular injury?
Tearing of the blood vessels of the brain = Type of traumatic head injury
After a blunt trauma to the back of the head, a patient has a black eye. Why is that?
=Basilar scalp fracture
Blood moves with gravity to eye orbits
What is meant by a Stellate laceration?
=splitting of the skin (common with falling backwards), and the fracture is NOT linear (in relation to head injuries)
What is the most common type of skull fracture?
Linear
What is a Depressed skull fracture?
=skull being pushed in aswell as fracturing
Define a Hinge skull fracture.
From the midline of the brain to the temporal bones
=usually presents with blood in the ear
~MOST COMMON IN: Road traffic incidents
Define a Pond / Ripple skull fracture.
Depressed type fracture in a child
What causes an Extradural haemorrhages and when would it present?
Usually due to impact to the side of the skull
=accumulate over time - will take minutes to hours before the raised intracranial pressure rises and gives rise to symptoms
-before symptoms arise = Lucid interval
pressure of blood pushes up against the brain and compresses it
What is the Lucid interval?
Is the period of no symptoms of a Extradural Haemorrhage (/Haematoma) before symptoms present (this is because it takes a while for the blood to accumulate)
=can present as if they are drunk
What is a key sign of a basal skull fracture?
Leaking of csf and blood in ear
Describe the pathophysiology of a Subdural haemorrhage.
Impact causes the brain floating in the CSF to cause tearing of bridging veins which empty into the superior saggital sinus
Who is most at risk of Subdural Haemorrhage / Haematoma and why?
-Elderly
-Alcoholics
=Their brains have shrunk which causes strain on the bridging veins so that very minor falls, the movement of the brain in the CSF can cause a subdural haemorrhage starting with confusion and leading to unconsciousness
-Huntington’s, Alzheimer’s, Amyloidosis
=Amyloid deposition makes a minor fall result in a major haemorrhagic event
What is meant by a Contrecoup fracture?
Bruising of the brain is opposite to the point of impact (e.g impact at the back causing the brain in the csf to whack the front of the skull so bruising will be at front)
=cerebral oedema
=pinching onto the pons which controls your breathing –> death
What are the consequences of a child falling down stairs vs adults falling
Bounce and won’t have significant injuries (e.g head trauma) compared with an adult, so if head trauma is present –>ABUSE
Where are the common sites for Cerebral contusions (contra-coup)?
Frontal lobes and Temporal poles
Where is contra-coup head injury less likely to happen?
Occipital lobe
What is the most common cause of Subarachnoid haemorrhage?
Berry Aneurysms
When would you most likely see a Traumatic diffuse axonal injury?
-road traffic collision
-fall from height
=usually present unconscious
=EXTREMELY LIFE THREATENING
What is meant by a Basilar Skull fracture?
Fracture to the base of the skull
=Usually caused by substantial blunt force trauma, involves at least one of the bones that compose the base of the skull, most commonly involving the TEMPORAL BONES but may involve the occipital, sphenoid, ethmoid, and the orbital plate of the frontal bone as well.
What is a contusion?
Bruise
What is laceration?
Cuts or tears of the skin
What is an incision?
Slash injury
What is a penetrating wound?
Stab wound
What is meant by a Sentinel Bleed?
Symptoms of headaches, dizziness and visual disturbances may precede a Subarachnoid Haemorrhage 2-3 weeks before due to an expansion of the aneurysm.
List the risk factors for a Subarachnoid Haemorrhage.
Smoking
Hypertension
Alcohol
Cocaine
Connective tissue diseases
Family History
What other illnesses is Berry Aneurysms associated with?
-Polycystic Kidney Disease
-Connective Tissue disorders
-Coarctation of the aorta
What investigations are required for a suspect Subarachnoid Haemorrhage?
1.CT without contrast
2.Angiography with a catheter = to localise bleed
3.IF CT NEGATIVE
=Lumbar Puncture (Detection of Xanthochromia confirms diagnosis i.e Yellow CSF)
What is a Subdural Haematoma?
Pooling of blood in the subdural space most commonly due to the rupture of bridging veins.
What type of head injury are Subdural Haemorrhages associated with?
Vigorous Coup and Counter-coup forces in NON ACCIDENTAL INJURIES IN CHILDREN
Compare a Subdural Haematoma with a Extradural Haematoma in terms of presentation?
Subdural:
Consciousness doesn’t fully recover and it gradually decreases with increasing confusion.
Other symptoms: Drowsiness, Incontinence
~Usually seen in the elderly
Extradural:
-LUCID INTERVAL
=Regain full consciousness but have an ongoing and severe HEADACHE
Other symptoms: Raised intracranial pressure symptoms (nausea, vomiting and visual problems)
–>Gradually lose consciousness
What type of haematoma / haemorrhage are you most likely to see a lucid interval in?
Extradural
When do you usually see an Extradural Haemorrhage?
The typical presentation is of a young patient involved in a head strike (either during sport or a result of a motor vehicle accident) who may or may not lose consciousness transiently
When do you usually see a Subdural Haemorrhage?
Typically due to falls or Non-accidental injuries in children
Compare the CT findings between a Extradural haematoma and a subdural haematoma.
Extradural: Lens-like appearance
Subdural: Crescent shaped haematoma
What is the management for a Subdural Haematoma?
Burr hole craniotomy haematoma evacuation
Where in the brain is usually affected by an Extradural Haematoma?
Middle Meningeal Artery in parietal or temporal bone fractures
What are the main causes of Raised intracranial pressure?
-Space occupying lesion in brain
-Infections
-Intracranial thrombosis e.g Extradural Haematoma
-CSF excess e.g Hydrocephalus
How does raised intracranial pressure present?
-Headache : Nocturnal or morning (upon waking) and WORSE ON COUGHING OR STRAINING
-Nausea and vomiting
-Visual issues
-Ptosis
-Cranial nerve 3 and 6 palsies
-Blurring optic disc
-Hyperaemia (increased blood flow to head)
-Papilloedema
What is Hydrocephalus?
Increase in the volume of circulating CSF within the cerebral ventricles
What are the 4 forms of Hydrocephalus?
1.Communicating
2.Non-communicating
3.Normal pressure
4.Hydrocephalus ex vacuo
What is meant by Communicating Hydrocephalus?
-Impaired absorption of CSF
-NO OBSTRUCTION to CSF flow within ventricles
What are the causes of Communicating Hydrocephalus?
-Subarachnoid Haemorrhage
-Meningitis
What is meant by Non-communicating Hydrocephalus?
Obstruction of CSF flow, due to congenital deformities (e.g Arnold-Chiari / Spinal Bifida/ Aqueduct stenosis) or acquired from bleeding, infections and tumours.
What is Normal pressure hydrocephalus?
When the Cerebral Ventricles are dilated.
How does Normal Pressure Hydrocephalus present?
-Urinary Incontinence
-Dementia
-Gait Disturbances =Magnetic (Feet seemingly stuck to the floor with small strides)
What investigations are required for Normal Pressure Hydrocephalus?
-MRI/CT
What is the management for Normal Pressure Hydrocephalus?
-Lumbar puncture
=remove large volume to provide short term improvement
-CSF shunting
=DEFINITIVE treatment
What is Hydrocephalus Ex Vacuo?
Brain atrophy (e.g Dementia) causes compensatory dilatation of the ventricles causing Hydrocephalus
What is the management for Hydrocephalus Ex Vacuo?
Drain / Shunt procedure (definitive treatment)
What is the treatment for hydrocephalus while waiting for definitive treatment?
-Mannitol / Hypertonic Saline as bolus = to cause osmotic diuresis and decrease CSF
-Treat Pyrexia and Seizures if present
What is the presentation of Idiopathic Intracranial hypertension and who is most likely to present with it?
1.Raised Intracranial pressure
-Morning/Nocturnal headaches
-Vomiting
-Pulsatile Tinnitus
-Papilloedema
2.Young, Obese, Pregnant
What is Cerebral Vein Thrombosis?
Aka CVT, when there is a blood clot in the brain
=Presents like a stroke / Intracranial Hypertension
List the risk factors for Cerebral Vein Thrombosis (CVT).
-oral contraceptives
-recent pregnancy
-infection.
-most common in females ages 30–41.
Describe the presentation of Cerebral Vein Thrombosis.
~50% of patients have SEIZURES
-Nausea and vomiting
-Loss of consciousness
-Focal neurology may develop depending on the area of the brain affected
What investigations are required to diagnose Cerebral Vein Thrombosis?
CT scan of head or MRI
D dimer levels
Antiphospholipid antibodies
What is the treatment for Cerebral Vein Thrombosis?
Anticoagulation ONLY ONCE HAEMORRHAGE HAS BEEN EXCLUDED
What does D dimer indicate and what is a worrying result?
The amount of clotting
>0.5 ~ thrombosis
What does Anosmia mean?
Partial or full loss of smell
A patient presents with seizures. What is the first diagnosis to exclude?
Space occupying lesion
What could be a Space occupying lesion in the brain?
-Tumour (or from metastasis)
-Haematoma
-Infiltration (infection)
-Abscess
A patient presents with anosmia. What lobe of the brain is most likely affected?
Frontal
A patient presents with behavioural changes. What lobe of the brain is most likely affected?
Frontal
A patient presents with dysphasia. What lobe of the brain is most likely affected?
Temporal lobe
Are brain tumours in adults usually Supratentorial or Infratentorial?
Supra
Are brain tumours in children usually Supratentorial or Infratentorial?
Infra
What is the treatment for Increased Cranial Pressure?
-Mannitol / Hypertonic saline
What is the most common brain tumour in adults?
Metastatic from lung and breast cancer
A patient has a suspected brain space occupying lesion. What are the next steps (investigations / management)?
-CT or MRI (MRI preferred)
-Treat underlying intracranial pressure (mannitol)
-Neurosurgical excision
What are the 2 most common forms of brain tumours?
-Glial (e.g Ependymomas, Astrocytomas)
-Meningiomas
What are risk factors for Multiple Sclerosis?
-Viral infections e.g Epstein Barre
-Lack of sunlight
-Vit D Deficiency
-HLA-DRB1
What is the pathophysiology of Multiple Sclerosis?
Inflammation, demyelination and axonal degeneration caused by CD4 cell mediated destruction of the oligodendrocytes (supporting neuronal cells) resulting in NEURONAL DEATH
Name a common type of brain tumour and its most aggressive form as well as its prognosis.
-Glial
=Glioblastoma Multiforme
1 year to live:(
What gene is linked to Multiple Sclerosis?
HLA-DRB1
What histological results would you expect from a patient with Multiple Sclerosis?
-Inflammatory cells :
-T cells
-B cells
-Macrophages
What is the most common form of Multiple Sclerosis?
Relapsing-remitting subtype (80-85% of cases)
What is meant by Relapsing-remitting Multiple Sclerosis?
Episodes of new or worsening symptoms, known as relapses that WORSEN OVER A FEW DAYS and last for days to weeks and then SLOWLY IMPROVE.
Describe a typical INITIAL presentation of someone with Multiple Sclerosis.
Visual:
-Optic Neuritis (Scotoma, Colour Desaturation and pain on eye movement)
Sensory:
-Loss of pain and temperature (Spinothalamic tract)
-Loss of vibration, light touch and proprioception (Spinocerebellar tract)
-Radicular pain
-Trigeminal neuralgia
-Tingling/Tightness/ Twisting/Burning/Tearing sensation
What does Radicular pain mean?
Pinching of the nerves at the root causes pain in back and hips, radiating down the LEGS.
Character of pain:
BURNING, or STINGING pain, Decreased sensation of the legs, Numbness and Tingling
Muscle weakness (in severe cases)
List the potential presentations of Multiple Sclerosis?
-Visual defects (most common)
-Sensory defects (most common)
-Motor defects
-Cerebellar defects
-Autonomic defects
-Fatigue
-Depression
List the potential visual defects of Multiple Sclerosis.
-Optic Neuritis
-Opthalmoplegia
-Bilateral Internuclear Opthalmoplegia
What is Opthalmoplegia?
Paralysis or weakness of any of the 6 muscles controlling the EYE MOVEMENTS
Presenting
-Inability to move eyes
-Ptosis
-Diploplia
-Blurry vision
-Strabismus (misalignment of eye(s))
What is Bilateral Internuclear Opthalmoplegia?
Movement disorder of the eye due to a lesion of the Medial Longitudinal Fasciculus affecting the ability of LATERAL GAZE:
Eye that abducts = NYSTAGMUS
Contralateral eye = NO MOVEMENT
What is Strabismus?
Misalignment of one or both eyes
What are the potential sensory defects of Multiple Sclerosis?
-Loss of pain and temperature (Spinothalamic tract)
-Loss of vibration, light touch and proprioception (Spinocerebellar tract)
-Radicular pain
-Trigeminal neuralgia
-Tingling/Tightness/ Twisting/Burning/Tearing sensation
What are the potential motor defects of Multiple Sclerosis?
-Upper motor neuron features (Spascisity in the legs more than arms, Hypertonia, Hyper-reflexia and Babinski
-Transverse Myelitis
What are the potential Cerebellar symptoms of Multiple Sclerosis?
-Ataxia
-Slurred speech
-Nystagmus
-Vertigo
What is Transverse Myelitis (incl presentation)?
=Idiopathic Inflammation of part of the spinal cord that is associated with infections and autoimmune diseases.
=Common symptoms are back or neck pain, weakness or sensation changes in the arms or legs, or loss of bladder or bowel control.
What are the autonomic potential symptoms of Multiple Sclerosis?
-Loss of bladder and bowel continence
-Erectile dysfunction
-Impotence
-Increased sweating
-Constipation
What are the investigations to be done for a suspect Multiple Sclerosis and what results would you expect?
1.MRI - taken 3 months apart
=Gandolinium-Enhanced Lesions (multiple little white plaques across the brain)
2.Lumbar Puncture
=IgG Oligoclonal bands in CSF
3.Evoked Potentials
=demonstrates neuronal delayed response
What is the treatment for acute exacerbation / worsening of symptoms of Multiple Sclerosis?
-Oral Prednisolone / IV Methyl Prednisolone
What is the treatment for preventing relapses of Multiple Sclerosis?
Disease Modifying Therapies:
(specifically for relapsing-remitting)
-Dimethyl Fumarate
-Teriflunomide
-Alemtuzumab
What is the treatment for symptomatic relief of fatigue for patients with Multiple Sclerosis?
Amantadine, CBT
What does Dyskinesia mean?
Involuntary movements (usually due to Parkinsons)
What is the treatment for symptomatic relief of depression for patients with Multiple Sclerosis?
Amitriptyline
What is the treatment for symptomatic relief of Neuropathic pain for patients with Multiple Sclerosis?
Choice of :
-Amitriptyline
-Duloxetine
-Gabapentin
-Pregabalin
What is meant by Lumbar spinal stenosis?
Narrowing of the central spinal cord causing back pain etc
What are the causes of Lumbar spinal stenosis?
-Tumours
-Prolapsed Discs
-Degenerative changes:
-Facet Joint Osteoarthritis
-Osteophytes formation
-Articular cartilage erosion (e.g sports injury)
=Causes mechanical compression and narrowing of the spinal canal
What are Osteophytes?
Bone spurs / bony lumps that grow on the bones in the spine or around joints usually due to arthritis.
What is the presentation of Lumbar Spinal Stenosis?
-Progressive back pain / lower limb pain (buttock pain is also possible), WORSE WHEN WALKING, BETTER WITH SITTING, LEANING FORWARD
-Numbness
-Paraesthesia
What does Paraesthesia mean?
Sudden burning or prickling sensation that is usually felt in the hands, arms, legs, or feet, but can also occur in other parts of the body.
Compare Neurogenic and Arterial Claudication.
Claudication is pain when walking causing a LIMP
=can be due to Peripheral Arterial disease or Neuronal compression
Can differentiate by:
-Neurogenic : Pain is positional (pain eased by leaning forward)
-Arterial : Peripheral pulses are diminished / absent
What investigations should be done for suspect Lumbar Spinal Stenosis?
MRI
What is the management of Lumbar Spinal Stenosis?
-Body weight reduction (lifestyle changes)
-NSAIDs and Physiotherapy
IF UNRESPONSIVE:
=Decompressive Laminectomy
What is Syringomyelia?
Development of a fluid-filled tubular cavitation within the spinal cord (usually the CERVICAL) portions.
Note: Think ‘Syringe’- as in a tube filled with liquid
What is the most common cause of Syringomyelia?
Obstruction of CSF flow
What congenital disorder predisposes someone to Syringomyelia?
Arnold Chiari
What is Arnold Chiari?
Congenital malformation causing the brain to push down on the spinal cord - life expectancy means unlikely to make it to childhood
What is the onset of Syringomyelia?
INSIDIOUS onset between 20-30years, rapid progression
What is the presentation of Syringomyelia?
Classical ‘cape-like’ loss f sensation of:
-Chest
-Shoulders
-Upper limbs
-Muscle weakness
What investigations are to be done for suspect Syringomyelia?
-MRI
What is the management of Syingomyelia?
Neurosurgical intervention:
-Shunt insertion
-Syringotomy and drainage
-Laminectomy
-IF ARNOLD CHIARI : Decompression of the malformation
What is Anterior Spinal Artery Syndrome?
Ischaemic event that causes a decrease in blood supply to the anterior 2/3rds of the spinal cord.
what is another name for Spinal Artery Syndrome?
Vertebrobasilar occlusion or Beck Syndrome
What is the presentation of Beck Syndrome?
-Loss of sensory input from anterior cord (Pain and Temperature)
What is the most common cause of Beck Syndrome?
Aortic pathology e.g Dissection / Aneurysm
What column is usually spared i.e unaffected by Syringomyelia?
Dorsal column
(therefore will retain proprioception and vibration)
What column is usually spared i.e unaffected by Beck Syndrome?
Dorsal column
(therefore will retain proprioception and vibration)
What is the prognosis of Beck Syndrome?
Permanently Paraplegic or Quadraplegic
What is Spondylosis?
Age-related degeneration of the spinal cord commonly caused by Osetoarthritis causing pain or sensinorimotor disturbances due to compression of the nerve
What is the management for Spondylosis?
Conservative - NSAIDs and Physiotherapy
What is Spondylolisthesis?
Anterior or Posterior displacement of vertebra due to usual wear and tear, arthritis
What is the management for Spondylolisthesis?
Conservative - NSAIDs
What is Brown-Sequard Syndrome?
Insult / Injury to the lateral half of the spinal cord affects the Corticospinal (movement of body) and Spinothalamic (vibration and proprioception, temperature and pain).
Very RARE ~ trauma
What is the presentation of Brown-Sequard Syndrome?
IPSILATERAL loss of
-Proprioception, vibration sense
CONTRALATERAL loss of:
-Pain and temperature
List the red flag symptoms in relation to back pain?
-Saddle Anaesthesia
-Bowel / Bladder dysfunction - incontinence
-Trauma
-Point tenderness / sudden onset
-Pain at night - waking from sleep
-History of malignancy
-History of IV drug missuse
-
What is Subacute Combined Degeneration of the cord?
Due to a deficiency in B12 / Folate : Degeneration the dorsal columns of the spinal cord (impairment of proprioception and vibration)
What illnesses cause Subacute Combined Degeneration of the cord?
-B12 deficiency
-Vit E deficiency
-Pernicious anaemia
-Malabsorption disorders (e.g IBS)
What does a flapping tremor indicate?
-Carbon dioxide retention
-Liver impairment (late-stage)
What is an essential tremor?
Most common type of tremor due to genetic link affecting mainly the upper limbs and can affect speech and tremor of the head (Titubation)
IMPROVES : With alcohol
WORSENS: When goal orientated, arms outstetched
NOTE: VERY RARE to tremor at rest
What does Titubation mean?
Tremor of the head
What is the treatment for an essential tremor?
-Propranolol or Primidone
List the causes of Parkinsonism.
-Multisystem Atrophy /Shy-Drager Syndrome
-Progressive Supranuclear Palsy
-Lewy Body Dementia
-Corticobasilar degeneration
-Vascular Parkinsonism
-Antipsychotic medication (e.g Metoclopramide, Prochlorperazine)
-Wilson Disease
-Chronic traumatic Encephalopathy
What does Parkinsonism mean?
Broadly encompasses several disorders (incl Parkinsons) that cause these HyPOkinetic symptoms :
-Resting tremor
-Bradykinesia
-Rigidity
What are the clinical presentations of Shy Drager Syndrome?
-Parkinsonism
-Speech disturbances
-Autonomic dysfunction (e.g bladder atony, postural hypotension)
What does Atony mean?
Loss of tone
What are the clinical presentations of Progressive Supranuclear Palsy?
-Parkinsonism
-Speech disturbances
-Personality changes
-Dementia
-Vertical Gaze Palsy
What are the clinical presentations of Lewy Body Dementia?
-Parkinsonism
-Deteriorating cognitive ability
-Visual Hallucinations
What are the clinical presentations of Corticobasilar degeneration?
-Parkinsonism
-Alien limb syndrome (limb movement without cognitive awareness)
-Apraxia
-Aphasia
What does Apraxia mean?
Disorder of planned motor performance e.g understands words but has difficulty articulating words
How does the cerebellum attach to the brainstem?
Cerebrum Peduncles
Where do the cranial nerves originate?
The brainstem
What are the deep structures of the Diencephalon?
-Thalamus
-Hypothalamus
-Third ventricle (CSF)
Name the 3 types of nerve fibres (between the hemispheres going to brain stem).
(Depending on where the axons are going)
1.Association fibres (intrahemispheric-stay in the same hemisphere)
2.Commisural (cross over the corpus callosum connecting the hemispheres)
3.Projection (leave and exit hemispheres and out of the brain stem and into the spinal cord)
What is the most important cell type in cerebral cortex?
Pyramidal cells (output neurons)
Stellate cells
Star shaped interneurones (single axons with lots of dendrites connecting neurons to one another within cerebral cortex)
What are the Cells of Martinotti?
long axon projecting to top of cerebral cortex
Pyramidal cells
Lots of dendrites varying in size - one of the biggest cells in the entire body
What are the 6 Layers of the cerebral cortex?
1.Molecular Plexiform layer (Afferent / Sensory : Synaptic layer)
2.External/ Outer granular layer(Afferent / Sensory : Predominance of Stellate interneurons)
3.External Pyramidal layer (Afferent / Sensory : Less densely populated but mainly has Pyramidal cells )
4.Internal / Inner Granular layer (stellate cells and nerve plexus to act as a barrier between the afferent (1-3) and efferent (5-6)
5.Internal Pyramidal / Ganglionic layer (efferent/ motor : Betz (type of pyramidal- very big)
6.Multiform cell layer (efferent / motor)
Note: That the thickness and dominance of the different layers will vary depending on where it is
e.g Sensory cortex of brain : Layers 1-3 will be thicker and in Motor cortex of the brain : Layers 5-6
Give examples of supporting neuronal cells giving rise to cancer.
Astrocytoma and Glioblastomas
What is the white matter in the Cerebellum?
Arbor vitae (tree like structure to increase surface area)
What is the grey matter in the Cerebellum?
Folia and Central Nuclei
What are the 3 layers of the Cerebellum
1.Molecular (axons and fibres here - lots of synaptic communication)
2.Central layer (Purkinje cell bodies here)
3.Inner granule layer (smaller nuclei present here)
What is the predominant cell type in the cerebellum?
Purkinje cells (large and expanding dendrites)
Spinal cord grey matter H shape structure- 3 main columns
1.Dorsal Horn / Posterior (afferent /sensory)
2.Lateral (Autonomic senses)
3.Ventral Horn / Anterior (Efferent / motor)
Anterior horn
in cervical, lumbar and sacral enlargement
=controls upper and lower limbs
anterior and posterior horn slim where?
thoracic level
Ascending (afferent) and Descending (efferent) tracts where are they present?
White matter (and then goes to grey)
Most common cause of Hydrocephalus in children / babies?
Intraventricular Haemorrhage (usually in premature babies as brain isn’t full developed)
Most common causes of hydrocephalus in adults?
Stroke of the cerebellar hemispheres, Tumours
Colloid cyst
benign lesions causing obstruction of CSF flow
Presentation of hydrocephalus in infants
Early signs are not obvious:
-Macrocrania (enlarged head)
-Vomiting / Poor feeding
-Abnormal cry
-Sunsetting eyes
If they go unchecked the pressure on the brain stem causes:
-Bradycardia
-Recurrent apnoea / pneumonia
Main first presenting symptom in children/ adults
early morning headaches, positional
Acute presentation of hydrocephalus
-headaches, vomiting
-Diplopia
-Cranial nerve palsies (3rd, 4th and 6th)
-Ataxia
-Incontinence
-Dementia
-Bradycardia
-Hypertension
Patient presents with headache and has a shunt, what are you most suspicious of?
Hydrocephalus
What is meant by Sunsetting eyes?
Sign of raised intracranial pressure where by the pupils are pointing downwards (can’t look up)
What is meant by shock?
Life threatening condition where there is impairment of oxygenation of numerous organs
Give examples of Ischaemic conditions.
-TIA
-Stable angina
-Intestinal angina / Mesenteric Ischaemia
Intermittent claudication
What is an Endarterectomy?
Removal of atheroma in the endothelium
-might be offered to a patient with an atheroma causing a TIA
What is meant by Vasculitis?
Group of diseases where there is inflammation of blood vessels due to idiopathic or autoimmune (don’t know cause)
Examples:
-Cutaneous vasculitis (vasculitis rash)
-systemic (multiple organs)
-Kidneys : Heilim F Purpura
-Vasculitis of brain = strokes (cause for younger people)
What is the most common cause of Haemorrhagic strokes?
Hypertension
What is meant by an Arteriovenous malformation?
A congenital abnormal tangle of arteries and veins within the brain or on the surface, INCREASING risk of bleeding
What genetic condition is known for increasing the risk Berry Aneurysms?
Autosomal dominant polycystic kidney disease
What does Congo Red positive deposition mean?
Amyloid deposition
What is the definition of Parkinson’s disease?
Neurodegenerative disorder characterised by resting tremor, rigidity and bradykinesia.
What is the pathophysiology of Parkinson’s?
Degeneration and loss of DOPAMINERGIC NEURONS in the SUSTANTIA NIGRA which is associated with accumulation of protein.
What protein accumulates in the Substantia Nigra in Parkinson’s disease?
Alpha-Synuclein protein
What is the difference between Bradykinesia and Hypokinesia?
Brady = slowness of movements
Hypo- absence of movements
What is the presentation of Parkinson’s?
1.Bradykinesia
2.Hypokinesia
3.Stiffness / Rigidity (lead pipe and cogwheel)
4.Pill rolling tremor resting tremor (improves on moving)
Give examples of signs of hypokinesia?
-Reduced facial expression
-Arm swing
-Blinking
-Slow, shuffling gait
-Difficulty to turn in bed
-Difficulty with fine movements e.g handwriting, buttoning clothes
What does micrographia mean?
-Difficulty with fine movements e.g handwriting, buttoning clothes
What are 3 specifically LATE signs of Parkinson’s Disease?
-Postural hypotension
-Tendency to fall backwards
-Dementia and psychosis
What is the criteria for diagnosing Parkinson’s?
Bradykinesia + one of the following:
-Muscular rigidity
-Fine rest tremor
-Postural instability
What is the first line management for a patient with Parkinson’s disease and what is the main consideration before prescribing?
Levodopa
-Whether their symptoms affect their daily life (don’t prescribe otherwise)
What is the management for patients with Parkinson’s when their symptoms aren’t severe?
Dopamine agonist (Pramipexole / Ropinirole)
A patient has been using Levodopa after their diagnosis of Parkinson’s yet they have developed motor fluctuations, what is the next management step?
Adjuvant therapy
e.g Entacapone or Tolcapone (Dopamine agonists)
What medication should be given with Levodopa to Parkinson patients to reduce peripheral side effects?
Dopa-decarboxylase inhibitors
e.g Carbidopa
What is the cause of Amyotrophic lateral sclerosis (ALS)?
Neurodegenerative disorder that is mainly idiopathic but 10% of cases are linked to familial causes (genes).
Describe a classical presentation of ALS.
-Lower motor signs in the upper limbs
-Upper motor signs in the lower limbs
-Progression of symptoms to other parts of the body e.g face (bulbar).
What is the least common type of onset of ALS?
Bulbar onset whereby the symptoms start in the face before the limbs
What is the management for ALS?
Riluzole (glutamate antagonist to slow progression of disease and lengthen lifespan)
-NOTE: NOT a cure
What is the leading cause of death in ALS patients?
Respiratory failure due to progressive muscle weakness and atrophy
List the cranial nerves.
Remember Mneumonic.
Oh Oh Oh To Touch And Feel Very Giant Volcanos Ahhh Hot!
- Olfactory (I)
- Optic (II)
- Oculomotor (III)
- Trochlear (IV)
- Trigeminal (V)
- Abducens (VI)
- Facial (VII)
- Vestibulocochlear (VIII)
- Glossopharyngeal (IX)
- Vagus (X)
- Accessory (XI)
- Hypoglossal (XII)
Which cranial nerves are motor, sensory or both?
Remember mneumonic.
Some Say Marry Money But My Brother Says Big Brains Matter More
I Sensory
II Sensory
III Motor
IV Motor
V Both
VI Motor
VII Both
VIII Sensory
IX Both
X Both
XI Motor
XII Motor
What is Progressive bulbar palsy?
Neurodegeneration of the nerves supplying the face presenting as facial weakness in swallowing, talking or chewing.
Is Progressive bulbar palsy lower or upper motor neurone issue and cranial nerves are affected?
Lower :
IX Glossopharyngeal
X Vagus
XII Hypoglossal
What are the key clinical signs of Progressive bulbar palsy?
-Absent jaw jerk / Gag reflex
-Tongue wasting
What is the management for progressive bulbar palsy?
No cure, just supportive
What is Pseudobulbar palsy and how is it different from progressive bulbar palsy?
Neurodegenerative UPPER motor (not lower as in Progressive bulbar palsy) affecting the face.
What cranial nerves are affected by Pseudobulbar palsy?
IX, X, XII
What are the clinical signs of Pseudobulbar palsy?
-Tongue muscles and speech are SPASTIC
-HYPER-reflexic of jaw jerk and gag reflex
What is Hereditary Spastic Paraplegia?
Group of genetic disorders causing progressive muscle SPASTICITY and disordered gait in LOWER limbs due to AXONAL DEGENERATION with varying levels of disability but NORMAL LIFE EXPECTANCY
What is meant by Hemisballismus?
Rare disorder causing LARGE INVOLUNTARY FLINGING MOVEMENTS of one half of the bodyWhat are t
he causes of Hemisballismus?
-Contralateral stroke
-Traumatic injury
-ALS
What is Benign Essential Myoclonus and what is the possible treatment?
Sudden involuntary twitching / jerks which is not present as a feature of other illnesses such as epilepsy usually presenting in childhood or adolescence
=Clonasepam or Sodium Valproate
What is the genetic cause of Huntington’s disease?
CAG triplet repetition found on the HTT (Huntington) Gene located on chromosome 4.
When is the usual onset of Huntingtons?
30-50s
What is the presentation of Huntington’s Disease?
-Depression (may be first sign)
-Chorea
-Poor coordination
-Dysarthria
-Dysphagia
-Jerky eye movements
What is meant by Chorea?
Abnormal involuntary movements (such as fidgeting, involuntary vocalisation etc)
What is the prognosis of Huntington’s?
20 years from onset of symptoms :(
What is the management of Huntington’s?
Benzodiazepines (for Chorea and depression)
What is the inheritance of Friedreich ataxia?
Autosomal recessive
What is the genetics of Friedreich ataxia?
Autosomal recessive mutation in the Frataxin gene on chromosome 9.
When is the onset of Friedreich ataxia?
Teens and twenties
Describe the typical presentation of Friedreich ataxia.
-Progressive ataxia
-Weakness
-Loss of proprioception and joint position
What disorders is Friedreich ataxia associated to?
-Pes Cavus
-Hypertrophic Cardiomyopathy
-Arrythmias
-Scoliosis
-Visual disturbances
-Diabetes Mellitus
What is meant by mononeuropathy?
Neuropathy affecting one particular nerve
What is meant by polyneuropathy?
Multiple nerves affected within a region
What is meant by mononeuritis multiplex?
Multiple nerves affected in different locations in the body
What medication is associated with the development of Peripheral Neuropathy?
Isoniazid (for TB)
Vincristine /Vinblastine (Chemotherapy)
List the disorders causing sensory peripheral neuropathy.
-Diabetes Neuropathy
-VitB12 deficiency
-Alcohol
-Leprosy
-Vasculitis
List the disorders causing motor peripheral neuropathy.
-Guillain-Barre syndrome
-Hereditary Sensorimotor neuropathies
-Lead poisoning
Give symptomatic examples of autonomic neuropathy.
-Urinary retention
-Impotence
-Sweating
-Sweating
-Tachy or bradycardia
-GI disturbances
What is the cause of Guillain-Barre syndrome?
Prior infection with Campyykibacter Jejuni.
What is the most common subtype of Guillain Barre in Asia?
Miller-Fisher syndrome
What antibodies are present in Miller Fisher syndrome?
Anti-GQ1b
What is the most common subtype of Guillain Barre syndrome (worldwide)?
Acute Immune Demyelinating Polyneuropathy
Who is most likely to be affected by Guillian Barre syndrome?
Men at the age of 40
List the clinical features of Guillain Barre Syndrome.
1.Weakness
=Symmetrical, Bilateral and Ascending (sensory) paralysis
2.Sensory disturbances
=Paraesthesia in distal extremities
=Absent or reduced motor reflexes (lower motor signs)
3.Pain
=Back, limb or neuropathic pain
4.Autonomic dysfunction
=Sweating, urinary retention etc
5.Respiratory muscle paralysis
Describe the weakness symptoms of Guillian Barre Syndrome.
-Symmetrical and Bilateral
-Ascending weakness
Where are the sensory disturbances felt in Guillian-Barre Syndrome?
Distal extremities (Hands and Feet)
How is Guillain-Barre Syndrome diagnosed?
Based on clinical observations
But if unclear:
+Pulmonary function tests
+Anti-ganglioside antibodies or GQ1B antibodies for Miller-Fisher
What is the management of Guillain-Barre?
-IV Immunoglobulin exchange
+Symptom control
A patient has Guillian-Barre. What is the criteria for admitting the patient to the Intensive Care Unit?
Flow Volume <1.5L
What type of drug can cause a delay in recovery from Guillian-Barre?
Corticosteroids
What is the prognosis for Guillian-Barre?
Great- most recover fully but 10% DIE from respiratory complications
What drugs are contraindicated in patients with Charcout-Marie-Tooth Disease?
-Isoniazid (TB)
-Vincristine (Chemotherapy)
What is Charcot-Marie-Tooth Disease?
Group of hereditary sensory AND motor neuropathies
What is the inheritance of Charcot-Marie-Tooth Disease?
Autosomal Dominant
What is the classical presentation of Charcot-Marie-Tooth Disease?
-Lower limb muscle weakness and wasting
-Champagne bottle legs (redness and compression above ankle to below knee looking like an inverted champagne bottle)
-Foot drop
-Small muscle wasting of the hand causing ‘claw hand’ (small fingers curled in)
-Pes Cavus
-Neuropathic pain
What is meant by Pes Cavus?
Abnormally high plantar longitudinal arch (i.e the arch of the foot between heel and toe is pronounced)
How is the diagnosis of Charcot-Marie-Tooth Disease confirmed?
Nerve conduction studies or genetic testing
What is the genetic pathology of Charcot-Marie-Tooth Disease?
Duplication mutation of the short arm of chromosome 17 effecting mitochondrial proteins which are required for axons and schwann cells for optimal nerve functioning
What is the pathophysiology of Myasthenia Gravis?
Autoimmune condition affecting the Acetylcholine receptors at the neuromuscular junctions due to attack by autoantibodies therby decreasing the regularity of action potenital generation causing progressive muscle weakness .
Who is most likely to suffer from Myasthenia gravis?
Women in their 30-40s
If men are affected by Myasthenia Gravis, what age is the usual onset?
60s (different from women)
What other disorders is Myasthenia Gravis associated with?
-Thymomas
-Thymic Hyperplasia
What is the classical presentation of Myasthenia Gravis ?
-Bilateral Ptosis or Diplopia
-Limb weakness or general weakness
-Myasthenic ‘snarl’ upon smiling
-Voice becomes softer counting to 50
=Better in mornings, worse in evenings and with exercise / activity
How is muscle tone, wasting and reflexes affected in Myasthenia Gravis ?
Not affected! :)
(because this isn’t an upper or lower, but a neuromuscular junction issue)
What can worsen symptoms of Myasthenic Gravis?
-Emotional distress
-Pregnancy
-Certain Medications
-Intercurrent disease (other disease at same time)
What symptoms are seen upon worsening and progression of Myasthenia Gravis ?
-Dysphagia
-Respiratory Compromise
What is Lambert Eaton Myasthenic Syndrome and how is different to Myasthenia Gravis ?
Another neuromuscular junction issue - Calcium channels affected in LE while Acetylcholine channels affected in MG
Remember mneumonic:
Early Learning Centre (Eaton Lambert - Calcium)
Make America Great Again (MyAsthenia Gravis - Acetylcholine)
What is strongly associated with Lambert-Eaton Myasthenic Syndrome?
Small Cell Lung Cancer
What test is done to differentiate between Myasthenia Gravis and Lambert Eaton Myasthenic Syndrome?
3,4 Diaminopyrodine treatment to detect antibodies to voltage gated calcium channels.
A patient comes into the emergency department with symptoms typical of Myasthenia Gravis. What is a simple test to detect your suspicions?
Ice test:
Ice held against patient’s eye should reduce ptosis has the cold reduces the breakdown of acetylcholine by acetylcholinesterase at the neuromuscular junction.
What is the diagnostic process for Myasthenia Gravis ?
-Autoantibody detection (85% of patients will have this)
-Pulmonary function tests
-CT scan of thorax (to exclude thymomas)
What is the management of Myasthenia Gravis ?
1.Pyridostigmine (anticholinesterase inhibitor)
=Improves muscle weakness
2.Immunosupression
–>Short term: Steroids
–>Relapses: Cyclosporin, Methotrexate, Azathioprine,
3.Conisder Thymectomy
What is meant by muscular dystrophies?
Genetic conditions causing progressive muscular weakness, degeneration and wasting.
What is the inheritance for Duchenne Muscular Dystrophy and where is the mutation?
X linked recessive
=mutation in the dystrophin gene (which is a protein required in muscles)
What is the difference in pathophysiology between Duchenne Muscular Dystrophy and Becker’s Muscular Dystrophy?
Duchenne is a complete ABSENCE of the Dystrophin protein while Becker’s is disordered production of the protein and therefore less severe.
When is the onset of Duchenne Muscular Dystrophy?
Before the age of 4
What is the presentation of Duchenne Muscular Dystrophy?
-Delayed milestones (e.g speech and language)
-Gait abnormalities
-Proximal myopathy and wasting
-Calf pseudohypertrophy
What is the Gower’s sign and what does it indicate?
When a child has to use their hands and arms to arrive at the standing position indicates Duchenne Muscular Dystrophy.
What is the diagnostic procedure for Duchenne Muscular Dystrophy?
Based on clinical observations
Note: Elevated Creatinine Kinase will be seen in bloods
What is the prognosis of Duchenne Muscular Dystrophy?
Poor, few patients survive past young adulthood :(
What is the mode of inheritance of Becker Muscular Dystrophy?
X linked recessive
What is the presentation of Becker Muscular Dystrophy and when is it usually diagnosed?
Similar presentation to Duchenne Muscular Dystrophy but LESS SEVERE.
=usually diagnosed in adolescence
What is the advice given to a patient with Becker Muscular Dystrophy?
Exercise regularly and optimise nutrition
What is a common complication of Becker Muscular Dystrophy?
Dilated Cardiomyopathy (enlarged heart chambers than can’t contract)
What is Myotonic Dystrophy?
Autosomal dominant disorder causing progressive muscle weakness and muscle wasting.
What additional tests should be done after a diagnosis of Becker Muscular Dystrophy?
Cardiovascular function test to check for Dilated Cardiomyopathy
What is the difference between type 1 and type 2 Myotonic Dystrophy?
Type 1 is congenital and SEVERE while type 2 is much milder
What is the presentation of Myotonic Dystrophy?
-Prolonged muscle contractions (impairment of muscle relaxation)
-Muscle wasting and weakness particularly head (TEMPORAL) and NECK
-Endocrine abnormalities (insulin resistance and fronto-temporal male pattern baldness)
-Heart block or Cardiomyopathy
What is Tuberous Sclerosis?
Autosomal Dominant causing both systemic and neurocutaneous abnormalities .
Describe the neuropathic pain in Multiple Sclerosis.
-Stabbing, tingling pain
-Feelings of being ‘hugged’ around trunk
What is the most common type of Multiple Sclerosis?
Relapsing-Remitting MS
(rather than Secondary Progressive)
Describe the pattern of Secondary Progressive Multiple Sclerosis.
-Follows initial course of Relapsing Remitting
-Constant symptoms that worsen
Note: This is the least occurent form
Name examples of Demyelinating disease.
-Multiple Sclerosis
-Neuromyelitis Optica
-Acute Disseminated Encephalomyelitis
Name 2 metabolic disorder differentials for Multiple Sclerosis.
-Vit B12 deficiency
-Adult-onset leukodystrophies
Name 2 infections that are differentials for Multiple Sclerosis.
-Lyme Disease
-Tropical Spastic Paraparesis
Name 2 systemic disorders that are differentials for Multiple Sclerosis.
Lupus
Sarcoidosis
What 2 malignant conditions are differentials for Multiple Sclerosis?
-Neostatic Brain Lesions
-Paraneoplastic syndromes
List the causes of folate acid deficiency.
-Medications
-Phenytoin (anti-convulsant)
-Methotrexate (Rheumatoid arthiritis)
-Pregnancy
-Alcohol excess
Describe the presentation of folate / B12 deficiency.
-Cognitive impairment
-Dementia
-Peripheral neuropathy
-Degeneration of the spinal cord
What is important to note when deciding on the treatment for a patient with both a folate and B12 deficiency?
Giving folate before B12 supplementation can cause a SUBACUTE DEGENERATION of the spinal cord (demyelination of the spinal cord worsening and causing severe neurological problems)
When are pregnant women considered high risk for their babies getting a neural tube defect?
-Phenytoin medication
-Methotrexate (Rheumatoid arthiritis and Chron’s disease)
-Coeliac disease
-Diabetes
-Thalassaemia
-Obese (BMI >30)
A pregnant woman is on Methotrexate for her Chron’s disease. What needs to be considered?
Methotrexate can increase risk of neural tube defect as it interferes with folate metabolism.
=5mg of folic acid prescribed to be taken on days when she doesn’t take her methotrexate.
What is the importance of Folate?
Involved in synthesis of neurotransmitters
What is the role of B12?
Involved in the production of myelin
Is Motor Neuron Disease upper or motor neuron disorder?
Mixture of both!
What is the most recognised side effect of Sodium Valproate?
Ataxia
What factors would indicate a poorer prognosis of Multiple Sclerosis?
-Age (older)
-Male
-motor signs at onset
-early relapses
-many MRI lesions and axonal loss
What is the only way to measure respiratory function in a patient with Guillian Barre?
Forced Vital Capacity at bedside
What are the signs of a cerebellar stroke? Remember mneumonic.
DANISH
Dysdiachokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
What is the first line treatment Myoclonic seizures?
Sodium Valproate
What is the Macula of the eye?
Important for Central vision
=Temporal to the optic disc where the blood vessels of the eye do not run
What is the clinical sign of Central Artery Occulsion seen on Fundoscopy?
Cherry red pot
Central artery occlusion, what happens and why?
As it is an end vessel, if there is a clot, it causes a Central Artery Occlusion (stroke of the eye)
What is the definition of Papilloedema?
A swollen optic nerve specifically due to raised intracranial pressure
What are the 2 layers of the retina (Retinal Pigmented Epithelium RPE) ?
Inner neural layer and outer pigmented layer
What treatment is regularly used for these common conditions-Macula degeneration, Diabetic Retinopathy ?
Intravitreol injection (through the vitreos of the eye specifically the Ora Serota)
Why is the Subretinal space (of the RPE) clinically important?
This is where water accumulates in Macula degeneration
What do the tight junctions of the RPE transport into the retina of the eye?
Glucose, Retinal, Phospholipids (for making photoreceptors)
How is light absorbed?
-A photon of light is absorbed by 11-cis retinal in the photoreceptors of the retina
-11-cis retinal changes to all-trans and free opsin
-All-trans is re-isomerised in the RPE
What does Opsin (of the eye) do?
Closes sodium channels to hyperpolarise and cause an action potential to produce vision
What does the RPE secrete?
VEGF promotes vascular leakiness
What is Optical Coherence Tomography used for?
Bio marker for retinal disease
=gives a histological like view of the retina without using a biopsy
=Offered to all Macula degeneration patients
What is the visual clinical sign of a Pituitary adenoma?
Bitemporal Hemianopia
=Temporal vision fields affected (outer vision fields)
Where do the optic nerves synapse?
Lateral Geniculate body
What is the clinical sign of an occlusion of the Optic nerve?
ONE eye complete loss of vision
What is the clinical sign of an occlusion from behind the optic chiasm?
Right Homonymous hemianopia
(same side of each eye)
When are Anti-VEGF injections commonly given?
Macula degeneration / diabetic eye disease (as it is due to an excess of VEGF)
so treatment = anti-VEGFs required to save vision
An MRI shows bilateral temporal hyperintensity. What does this indicate?
Herpes Simplex Virus causing Encephalitis
Causes of conductive deafness ?
-Wax
-Ruptured tympanic membrane
-Otitis Media (e.g with Labyrinthitis)
-Otosclerosis (sclerotic process which fuse the malleus and incus together so that they can no longer vibrate)
Causes of sensorineural deafness?
-Cochlea degeneration from ageing
-Sound pollution
-Meniere’s disease
-Acoustic Neuroma
-Tumours (VERY RARE)
Rinnes and Weber’s test: Sensorineural vs Conductive
Normal : Air better than bone conduction
Conductive: Rinnes -ve = Bone>Air
Weber=hearing better in one ear
Sensorineural: Rinnes +Ve = Air>Bone
Weber=
What frequencies are lost in Sensorineural vs Conductive hearing loss?
Sensorineural: high frequencies
Conductive: generalised frequencies
Is dilation and constriction due to Para, or Sympathetic innervation?
Sympathetic - dilates
Parasympathetic - constricts
Is Horner’s Syndrome ipsilateral or contralateral?
Ipsilateral
Define mania
Causes of mania
-Prednisolone
-Cocaine
-Ecstasy
-HIV
-Huntingotons
-MS
MND
-Hyperthyroidism
Typical presentation of bipolar disorder
psychiatric symptoms of tumours
-older (can indicate and diff from bipolar)
-any general psych pres
Responding to hallucinations
acute psychosis
Intoxication (Amphetamine/Cocaine/Meth)
abrupt severe psychological presentation
=Benzodiazepines and supportive environment
What neurotransmitter is behind psychosis usually?
Dopamine
catatonic symptoms
-Mutism- not talking for hours on end
-Catalepsy - bizarre postures that they will hold for hours
-Stupour (inmobility) AND/OR Motor excitement
-Echolalia =repeat what you say
-Echopraxia = copy your movements
Autoimmune Encephalitis antibodies
1.Look for antibodies (anti-NMDAR)
2.Sometimes won’t show up so do a lumbar puncture for DEFINITIVE DIAGNOSIS
Treatment
acute confused state
Withdrawl states
Pregabalin
Benzodiazepines
Alcohol
Withdrawal states symptoms
Causes of catatonia
1Neurological causes
-Autoimmune encephalitis
-CNS infection
-Metabolic disturbance
-Withdrawl state
2.Schitzoprenia
First line investigations for psychiatric-like presentation.
Rule out neurological causes
-Bloods (anti-NMDAR
-MRI
-EEG
-Lumbar puncture
Treatment for Catatonia
-Lorazepam challenge (high dose: 8-16mg)
-If it doesn’t work: ECT
Neurotic personality
Always anxious and particular
Medication Causes of anxiety
-Dominergic agents (parkinsons)
-Phenytoin
-B2 agonists (salbutamol)
-Stimulants (Phenylephrine for adhd)
-Thyroxine
Conditions causing anxiety
-Complex partial seizures
-Dementia
-Migraine
Arrhythmias
Mitral valve prolapse
Pulmonary Emboli
Phaeochromocytoma
Hypoglycaemia
Hyperthyroidism
Reversible causes of dementia
B12 and folate
Hypothyroidism
Wilson’s disease (serum copper)
HIV
Syphilis serology
Chronic alcoholism (Korsokoff syndrome)
Delirium vs Dementia vs Psychosis
Delerium is abrupt and consciousness fluctuates with prominent VISUAL HALLUCINATIONS which is not like Dementia (no visual and it is constant throughout the day)
Visual hallucinations
Not common feature so points to organic cause (underlying condition)
Multiple Sclerosis
dperession and anxiety
Post ictal
~Temporal epilepsy
=suicidal and high risk of violence
Parkinsons
visual and auditory hallucinations
psychosis
Vast majority are auditory hallucinations so otherwise points to neurological
Confusion / disorientation points to neurological as this is not present in psychiatric illnesses
Age of onset
younger
(older points to neurological)
First presentation of psychosis investigations
MRI/CT head and EEG
Dissociative neurological symptoms / Conversion disorder
Any psychiatric symptom which is related to physical injury or childhood abuse /neglect
Fugue
Amnesia - no memory and turns up somewhere else
Semantic memory
Facts
Dissociative Amnesia
Acute onset of memory loss after traumatic events
Hydochondriacal disorder
-overriding preoccupation of health worry
Management for Hypochondriacal disorder
CBT
Chronic Fatigue
Not really known
~ Viruses (EBV, Herpes)
~Psychological trauma
~IBS
~Fibromyalgia
What is a Functional Neurological disorder?
Neurological symptoms that can’t be explained and are reversible e.g seizures
What is meant by functional seizure?
Seizures do to psychological cause that can go on for a long time and not cause any damage
Triggers for Functional Neurological disorder?
-Illness
-Traumatic event
What is meant by a Functional tremor ?
High amplitude tremor that can stop with distractions
I.e caused by psychological issues rather than a condition such as Parkinson’s
What drugs can cause Drug induced Parkinson’s?
Causes:
Schitzophrenia - antipsychotics (Haloperidol)
Prochlorperazine - long term vertigo
When is parkinson’s referred as genetic and not sporadic/idiopathic?
First-degree relative or early onset
How to tell between drug induced and idiopathic parkinsons?
DAT scan in idiopathic will have neurodegeneration while drug induced will be normal (as all that is affected is dopmine blockade rather than neurodegeneration)
What is meant by Lewy Body Dementia?
triad of dementia, parkinsonism and visual hallucinations
Atypical Parkinsonism
Doesn’t respond to levodopa and therefore has a high mortality rate and lower prognosis
Deep brain stimulation for Parkinsons
(also look into what the NICE guidelines / indications are in the uk)
Subthalamic Nucleus targeted
Delusion definition
Fixed false belief without reason
Delerium
Acute fluctuating disturbance of attention and awareness with impairment in cognition
Hallucinations
PEricieved without stimuli
Psychosis
All of the above (delusion, delerium and hallucinations)
Meaning of extracampine
presence always with them (not always negative could be positive like a dead parent so wouldn’t be treated)
