Neurology Flashcards
what lobe?
seizure
Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing/plucking), Deja vu/Dysphasia post-ictal)
Temporal lobe (HEAD)
What lobe seizure?
Head/leg movements, posturing, post-ictal weakness, Jacksonian march
Frontal lobe (motor)
what lobe seizure?
paraesthesia
Parietal lobe (sensory)
what lobe seizure?
floaters/flashes
Occipital lobe (visual)
Brain scan where does encephalitis classically affect
temporal lobe
Hypsarrhythmia on EEG
Infantile spasms (west’s syndrome)
What birth defects are sodium valproate associated with
neural tube defects
hypospadias most common
epilepsy management pregnancy
aim for mono therapy
lamotrigine is often best choice
5mg folic acid prior to getting pregnant if possible
Normal lumbar puncture result
clear appearance
glucose 70% of plasma
protein 0.3 g/l
WCC 2 per mm^3 (neuts)
Bacterial meningitis LP result
Cloudy
Glucose low (< 1/2 plasma) bacteria using up the glucose
Protein high (> 1 g/l) bacteria releasing proteins
WCC 10 - 5,000 polymorphs/mm³ the immune system releases neutrophils in response to bacteria
Viral meningitis LP result
Clear/cloudy
Glucose 60-80% of plasma glucose* viruses don’t really use glucose
Protein normal/raised viruses may release a small amount of protein
WCC 15 - 1,000 lymphocytes/mm³ the immune system releases lymphocytes in response to viruses
Tuberculous LP result
Slight cloudy, fibrin web
glucose Low (< 1/2 plasma)
Protein high >1g/l
WCC 30-300 lymphocytes/mm3
The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)
Management of brain abscess?
surgery - craniotomy
IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
intracranial pressure management: e.g. dexamethasone
EEG : 3Hz generalized, symmetrical
absence seizures
EEG centro-temporal spikes
Benign rolandic epilepsy
Contraindications to lumbar puncture
focal neurological signs
papilloedema
significant bulging of the fontanelle
disseminated intravascular coagulation
signs of cerebral herniation
For patients with meningococcal septicaemia a lumbar puncture is contraindicated - blood cultures and PCR for meningococcus should be obtained.
Degenerative cervical myelopathy
Presentation: myelopathy: pain (affecting the neck, upper or lower limbs) loss of fine motor function (dexterity, clumsy) loss of sensory function causing numbness, loss of autonomic function, hoffmans
Causes: Cervical spondylosis (osteophyte), disc herniation
Investigation: MRI
Management: decompressive surgery
Neoplastic spinal cord compression
Presentation: cancer patient, back pain, bilateral weakness, UMN signs. First symptom: back pain
Investigation: MRI of whole spine
Management: high dose dexamethasone and oncology assessment
Brown-sequard syndrome
- ipsilateral dorsal column signs
- ipsilateral corticospinal tract signs
- contralateral spinothalamic tract signs
Subacute combined degeneration of spinal cord
Presentation: bilateral dorsal column signs, may have bilateral corticospinal tract signs (affects posterior cord)
Cause: B12 deficiency
Prevention: Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord
Friedrich’s ataxia
Presentation: teenage corticospinal, spinocerebellar, dorsal column and peripheral nerves
Information: autosomal recessive trinucleotide repeat disorder resulting in reduced level or function of the frataxin protein.
Investigation: genetic analysis
Management: supportive
Syringomyelia
Pathophysiology: development of a fluid-filled cyst (a syrinx) around the spinal canal.
Causes: Chiari malformation, tumour, trauma
Presentation: ‘central cord syndrome’ bilateral spinothalamic and/or bilateral corticospinal tract symptoms. The upper limbs are affected first whilst the lower limbs are spared until much later. As the fibres of the spinothalamic tract enter the spinal cord and immediately decussate, they pass close to the spinal canal, meaning they are often the first of these white matter fibres to be compressed and damaged. As the cervical cord is the most likely location of the lesion, there is classically said to be a “cape-like” loss of pain and temperature sensation.
Investigation: full spine MRI with contrast and brain MRI
Management: treat cause. If persistent : shunt
Lumbar spinal stenosis
Presentation: back pain, bilateral leg weakness or unilateral, positional element: better on walking up hill and sitting forward. Ddx claudication
Investigation: MRI
Management: Laminectomy
Ankylosing spondylitis
Presentation: young man, lower back pain and stiffness, worse in morning
Investigation: plain x ray of sacroiliac joints
Management: encourage regular exercise such as swimming, NSAIDs are the first-line treatment, physiotherapy
Myelopathy vs radiculopathy
Myelopathy: bilateral as spinal cord and bladder/bowel, not always painful “clumsiness” “loss of manual dexterity”
Radiculopathy: radiating limb pain, often in the pattern of the dermatome, sharp/shooting in character, with only a small proportion (about 5%) having associated neurologic symptoms such as dermatomal sensory loss, and even less commonly myotomal muscle weakness.
Myotomes upper limb
C5 – Elbow flexion (and shoulder abduction)
C6 – Wrist extension (and shoulder adduction) (and elbow flexion)
C7 – Elbow extension (and wrist flexion)
C8 – Finger flexion and thumb extension
T1 – Finger abduction
Myotomes lower limb
L2 – Hip flexion
L3 – Knee extension
L4 – Ankle dorsiflexion
L5 – Great toe extension
S1 – Ankle plantarflexion
Dermatome Thumb + index finger
C6
Dermatome middle finger + palm of hand
C7
Dermatome ring + little finger
C8
Dermatome nipples
T4
T4 at the Teat Pore
Dermatome xyphoid process
T6
Dermatome umbillicus
T10
BellybuT-TEN
Dermatome inguinal ligament
L1
L for ligament, 1 for 1nguinal
Dermatome knee caps
L4
Down on aLL fours - L4
Dermatome big toe, dorsum of foot (except lateral aspect)
L5
Largest of the 5 toes
Dermatome Lateral foot, small toe
S1
the smallest 1
Dermatome genetalia
S2, S3
Cauda equina most common cause
central disc prolapse at L4/5 or L5/S1
Parkinsons disease tremor
Unilateral resting tremor (improves with voluntary movement)
Causes of drug-induced parkinsonism
Antipsychotics or antiemetic metoclopramide can cause EPSE.
In patients with parksinons, prescribe antiemetic domperidone as it doesn’t cross BBB therefore doesn’t cause EPSE
Invetsigation lewy-body
SPECT/DaTSCAN
Glasgow coma scale components and scoring
Glasgow coma scale (GCS) out of 15
Motor response
6. Obeys commands
5. Localises to pain
4. Withdraws from pain
3. Abnormal flexion to pain (decorticate posture)
2. Extending to pain
1. None
Verbal response
5. Orientated
4. Confused
3. Words
2. Sounds
1. None
Eye opening
4. Spontaneous
3. To speech
2. To pain
1. None
MRC power grades
Grade 0
No muscle movement
Grade 1
Trace of contraction
Grade 2
Movement at the joint with gravity eliminated
Grade 3
Movement against gravity, but not against added resistance
Grade 4
Movement against an external resistance with reduced strength
Grade 5
Normal strength
Reflex nerve roots
Ankle = S1
Miss out 2
Knee = L3,4
Brachioradialis = C5,6
Biceps = C5,6
Triceps = C7
Causes and ddx features cranial third nerve palsy
Surgical third nerve palsy : painful, dilated pupil
- posterior communicating artery aneurysm
Diabetes : not painful, reactive pupil
Bell’s palsy
presentation and management
lower motor neuron facial nerve palsy - forehead affected
oral prednisolone within 72 hours
if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT
When should IV thrombolysis with mechanical thrombectomy be offered for ischaemic stroke?
Thrombectomy within 6 hours of onset
Thrombolysis within 4.5 hours onset
Both if occlusion if proximal anterior circulation on CTA or MRA
Wernikes aphasia
Presentation
Location
Receptive aphasia
Fluent speech, doesn’t make any sense, comprehension impaired
Lesion in superior temporal gurus
Supplied by inferior division of left MCA
Brocas aphasia
Presentation
Location
Blood supply
Non-fluent laboured and halting speech. Repetition impaired (expressive)
Inferior frontal gyrus
Superior division of left MCA
Spoken word is heard at the ear. This passes to Wernicke’s area in the temporal lobe (near the ear) to comprehend what was said. Once understood, the signal passes along the arcuate fasciculus, before reaching Broca’s area. The Broca’s area in the frontal lobe (near the mouth) then generates a signal to coordinate the mouth to speak what is thought (fluent speech).
Conduction aphasia
Presentation
Location
Speech fluent but repetition is poor
Aware of errors
Arcuate fasiculus (connection between brocas and wernikes)
Spoken word is heard at the ear. This passes to Wernicke’s area in the temporal lobe (near the ear) to comprehend what was said. Once understood, the signal passes along the arcuate fasciculus, before reaching Broca’s area. The Broca’s area in the frontal lobe (near the mouth) then generates a signal to coordinate the mouth to speak what is thought (fluent speech).
UMN signs
Minimal muscle atrophy
Weakness ‘Pyramidal’ pattern i.e. weakness of upper limb extensors, lower limb flexors So upper limb is flexed and lower limb extended (think hemiplegic gait)
Slightly reduced power
Hyperreflexia of deep tendon reflexes- as no UMN regulating that reflex
Absent superficial reflex - babinski positive
Hypertonia + or - clonus (Spasticity occurs in pyramidal tract lesions) such as clonus and clasp-knife rigidity
Pronator drift
management of extradural hematoma
stabilising the patient followed by surgical intervention with a burr hole or craniotomy to evacuate the haematoma.
blood vessel implicated by extradural hematoma
middle meningeal artery
eminem getting hit by a lemon
ct scan subdural hematoma
concave crescent-shaped
blood vessel implicated in subdural hematoma
bridging veins
old man drinking alcohol in a cave with a bridge outside and a crescent moon in the sky
management subdural hematoma
Small or incidental acute subdurals can be observed conservatively.
If big or signs then surgical options include monitoring of intracranial pressure and decompressive craniectomy.
Causes SAH
Ruptured cerebral aneurysm or trauma
conditions associated with berry aneurysms
adult polycystic kidney disease
Ehlers-Danlos syndrome
Coarctation of the aorta
ct scan for SAH
Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.
may be normal - do LP
lumbar puncture for SAH
LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown).
Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).
As well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure
invetsigation after spontaneous SAH confirmed?
CT intracranial angiogram
Management SAH
- referral to neurosurgery after confirmation
- coil by interventional radiologists
- or craniotomy
- 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature)
- Hydrocephalus is temporarily treated with an external ventricular drain
treatment of radiculopathy
Similar to that of other musculoskeletal lower back pain: analgesia, physiotherapy, exercises
If symptoms persist after 4-6 weeks then referral for consideration of MRI is appropriate
narcolepsy associations
associated with HLA-DR2
it is associated with low levels of orexin (hypocretin), a protein which is responsible for controlling appetite and sleep patterns
early onset of REM sleep
features narcolepsy
typical onset in teenage years
hypersomnolence
cataplexy (sudden loss of muscle tone often triggered by emotion)
sleep paralysis
vivid hallucinations on going to sleep or waking up
investiagtions narcolepsy
multiple sleep latency EEG
polysomnography
management narcolepsy
daytime stimulants (e.g. modafinil) and nighttime sodium oxybate
what CN palsy may be present in IIH
6th
Contralateral hemiparesis and sensory loss, lower extremity > upper
Anterior cerebral artery
Contralateral hemiparesis and sensory loss, upper extremity > lower, Contralateral homonymous hemianopia, Aphasia
Middle cerebral artery
Contralateral homonymous hemianopia with macular sparing, Visual agnosia
Posterior cerebral artery
Ipsilateral CN III palsy, Contralateral weakness of upper and lower extremity
Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain)
Ipsilateral: facial pain and temperature loss, Contralateral: limb/torso pain and temperature loss, Ataxia, nystagmus
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
Ipsilateral: facial paralysis and deafness
vertigo and vomiting
Anterior inferior cerebellar artery (lateral pontine syndrome)
a curtain coming down over their vision and episodes often recur.
Retinal/ophthalmic artery- Amaurosis fugax is a term used to describe transient monocular visual loss due to atherosclerosis of the ipsilateral internal carotid artery which causes lack of blood flow to central retinal artery
complete paralysis of voluntary muscles, very low GCS
Basilar artery- locked in syndrome
contralteral symptoms: either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
“Lacunar strokes - common sites include the basal ganglia, thalamus and internal capsule
“
contralateral hemiparesis/hemisensory loss of face arma dn leg, higher cog dysfunction such as aphasia, homonymous hemianopia
total anteroir ciruclation infact, if only 2 = partial
Bitemporal hemianopia
Midline lesion at chiasm
upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
Right nasal hemianopia
Lesion involving right perichaismal area
Left homonymous hemianopia
Lesion or pressure on right optic tract (posterior to chiasm, before optic radiations)
Lesion or pressure across all right optic radiations
Left homonymous hemianopia with macular sparing
Lesion in right occipital lobe (both banks of calcarine fissure) posterior cerebral artery
Left superior homonymous quadrantanopia
PITS = parietal inferior, temporal superior therefore;
Temporal as superior
Right sided tract
Lesion to the right inferior optic radiations in the temporal lobe (meyer’s loop)
Right inferior homonymous quadrantanopia
PITS = parietal inferior, temporal superior therefore;
Parietal as inferior
Right visual field so left optic tract
Lesion to the left superior optic radiations in the parietal lobe
“A 23-year-old man was driving a car at high speed whilst intoxicated, he was wearing a seat belt. The car collides with a brick wall at around 140km/h. When he arrives in the emergency department he is comatose. His CT scan appears to be normal. He remains in a persistent vegetative state.”
diffuse axonal injury
if they also have a bleed it will be subdural
About 90% of survivors with severe diffuse axonal injury remain unconscious. The 10% that regain consciousness are often severely impaired.
Management
Preventing secondary brain injury eg swelling etc.
“A 25-year-old male is brought to the emergency department after being struck on the side of the head with a bottle in a nightclub. According to one of his accompanying friends, he was knocked unconscious initially but then regained consciousness. An ambulance was called after the patient lost consciousness again. The admission CT head scan shows an intracranial haemorrhage.”
extradural hematoma
hypersensitive in bi-convex/lentiform brain ct
extradural hematoma
lemon shape (lemon thrown at head)
bi-convex - if youre vexxed you puff out in anger
“A 59-year-old man attends his GP with increasing mild confusion. This came on 2 weeks ago and has been getting progressively worse, both in his and his husband’s opinion. His past medical history is significant for being in a road traffic collision 6 weeks prior. At the time, he was discharged from the emergency department with no injuries but did suffer a head injury. Since then, he reports no headache, nausea or changes in vision.”
subdural hematoma
slow onset, fluctuating conscioussness/confusion
Sudden onset occipital headache (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’
Nausea and vomiting
Meningism (photophobia, neck stiffness)
subarachnoid haemorrhage
A 54-year-old man attends the GP complaining of double vision. He says it is worse when he walks down the stairs.
On inspection, he is sitting with his head tilted towards the right. The left eye deviates supero-laterally.
left trochlear never palsy
head tilt away from lesion.
Palsy results in defective downward gaze → vertical diplopia.
Palsy results in defective abduction → horizontal diplopia
abducens (6th) nerve palsy
uvula deviation and loss of gag reflex
vagus nerve
uvula deviates away from lesion
tounge deviation
cranial nerve 12
tounge deviates towards lesion
isolated foot drop and may have sensory loss on dorusm of foot
common peroneal nerve palsy
conservative management is appropriate. Leg crossing, squatting and kneeling should be avoided. Symptoms typically improve over 2-3 months.*
Sensory loss dorsum of foot
Weakness in foot and big toe dorsiflexion (foot drop)
Reflexes intact
Positive sciatic nerve stretch test
Hip abductors are also likely to be weak (superior gluteal nerve).
L5 radiculopathy
Sensory loss over anterior thigh
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test
L3 radiculopathy
Sensory loss anterior aspect of knee
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test
L4 radiculopathy
Sensory loss posterolateral aspect of leg and lateral aspect of foot
Weakness in plantar flexion of foot
Reduced ankle reflex
Positive sciatic nerve stretch test
S1 radiculopathy
Management of generalised tonic-clonic seizures?
males: sodium valproate
females: lamotrigine or levetiracetam
girls aged under 10 years and who are unlikely to need treatment when they are old enough to have children or women who are unable to have children may be offered sodium valproate first-line
Management focal seizures?
first line: lamotrigine or levetiracetam
second line: carbamazepine, oxcarbazepine or zonisamide
Management of absence seizures?
first line: ethosuximide
second line:
male: sodium valproate
female: lamotrigine or levetiracetam
carbamazepine may exacerbate absence seizures
Management atonic seizures?
males: sodium valproate
females: lamotrigine
What epilepsy syndrome benefits from ketogenic diet?
Lennox-Gastaut syndrome
Management juvenile myoclonic epilepsy/myoclonic
males: sodium valproate
females: levetiracetam
Management infantile spasms (west syndrome)
- Prednisolone or Vigabatrin
Star sign
SAH
Sciatic vs femoral tests?
The femoral nerve is for the front of the leg, while the sciatic nerve serves the back of the leg.
therefore femoral stretch test stretches the front of the leg (patient prone, knee at 90 degrees, lift up)
sciatica test (straight leg raise) stretches the back of the leg (patient supine, lift leg to elicit pain)
Bacterial meningitis 0-3 months
BELS
- Group B Streptococcus (most common cause in neonates)
- E. coli
- Listeria monocytogenes
- Strep pneumoniae
Bacterial meningitis 3 months-6 years
- Neisseria meningitidis
- Streptococcus pneumoniae
- Haemophilus influenzae
Bacterial meningitis 6-60 years
- Neisseria meningitidis
- Streptococcus pneumoniae
Bacterial meningitis >60 years
- Streptococcus pneumoniae
- Neisseria meningitidis
- Listeria monocytogenes
Meningitis in immunocompromised
listeria monocytogenes
Children in community meningitis initial management
Benzylpenicillin IM or IV
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
Meningitis initial empirical therapy < 3 months
IV cefotaxime + amoxicillin (or ampicillin)
Meningitis initial empirical therapy 3 months-50 years
IV cefotaxime
Meningitis initial empirical therapy > 50 years
IV cefotaxime + amoxicillin (or ampicillin)
Meningitis management - listeria
IV amoxicillin (or ampicillin)
+ gentamicin
When should dexamethasone be given for meningitis
Give if lumbar puncture reveals:
- frankly purulent CSF
-CSF white blood cell count greater than 1000/microlitre
- raised CSF white blood cell count with protein concentration greater than 1 g/litre
- bacteria on Gram stain
Withhold if:
- septic shock
- meningococcal
- septicaemia
immunocompromised
Management meningococcal meningitis
IV benzylpenicillin or cefotaxime
Post exposure prophylaxis bacterial meningitis
Ciprofloxacin single dose
This risk is highest for people that have had close prolonged contact within the 7 days prior to the onset of the illness
Most common pathogen encephalitis in children and adults
herpes simplex HSV-1 from cold sores
Most common pathogen encephalitis in neonates
herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth.
think “been passed on 2”
Management ?encephalitis
aciclovir (covers HSV and varicella zoster)
Management CMV encephalitis
Ganciclovir
Recurrent, non-disabling, bilateral headache, often described as a ‘tight-band’
Not aggravated by routine activities of daily living
tension headache
Recurrent, severe headache which is unilateral and throbbing in nature. Associated with nausea and photosensitivity. Last 4-72 hours
Behaviour: withdrawal, not moving, dark room, no noise
migraine
Migraine triggers
Chocolate
Hangovers
Orgasms
Cheese
Caffeine
The oral contraceptive pill
Lie-ins
Alcohol
Travel
Exercise
migraine diagnostic criteria
At least 5 attacks
Headache attacks lasting 4-72 hours* (untreated or unsuccessfully treated)
Headache has at least two of the following characteristics:
1. unilateral location*
2. pulsating quality (i.e., varying with the heartbeat)
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
During headache at least one of the following:
1. nausea and/or vomiting*
2. photophobia and phonophobia
acute management migraine
- Oral triptan + NSAID/paracetamol
- metoclopramide or prochlorperazine and non-oral NSAID or triptan
mechanism triptan
5-HT agonist
who should get prophylaxis for migraines
> 2 attacks per month
Migraine prophylaxis
- Topiramate or propranolol (propranolol for women of CBA as topiramate can be teratogenic and can reduce effectiveness of hormonal contraception)
- Acupuncture
- Riboflavin (vit B2) 400 mg may be effective at reducing migraine frequency and intensity for some people
Management of pre-menstrual migraines
Frovatriptan (2.5mg twice a day) or zolmitriptan (2.5mg twice or three times a day) as mini-prophylaxis
What type of side effects can occur in children and young adults taking antiemetic metoclopramide?
EPSE
Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks ‘always’ affect same side)
Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling
cluster headache
triggers for cluster headaches
alcohol
nocturnal sleep schedule
Acute management cluster headache
- 100% high flow oxygen (80% response within 15 mins)
- subcutaneous triptan (75% response within 15 mins)
When are triptans contraindicated
triptans are contraindicated in CAD as it may cause vasospasm
Prophylaxis cluster headaches
Verapamil
prednisolone
Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%)
(worse when talking for a while, worse when chewing, worse when moving jaw, tender to touch, scalp tenderness, worse when brushing hair, shaving etc)
Tender, palpable temporal artery
Visual disturbance
temporal arteritis
association temporal arteritis
50% have features of PMR : aching, morning stiffness in proximal limb muscles
Investigations temporal arteritis
Tender palpable temporal artery
Raised ESR >50 (10% of pts don’t have)
CRP may be elevated
Vision testing
Temporal artery biopsy : skip lesions (Histology shows changes that characteristically ‘skips’ certain sections of the affected artery whilst damaging others.) may also be normal
Management temporal arteritis
Urgent, no vision loss:
High dose oral glucocorticoids eg oral methylprednisolone
Urgent, vision loss:
IV methylprednisolone
What do you need to test in temporal arteritis? what may you find?
VISION
Amaurosis fugax
Blurring
Double vision
Severe unilateral pain, often triggered by touching the skin, brief electric shock like pains, abrupt in onset and termination
trigeminal neuralgia
Management trigeminal neuralgia
Carbamazepine
management Herpes zoster ophthalmicus (HZO)
oral antiviral treatment for 7-10 days
ideally started within 72 hours
topical corticosteroids may be used to treat any secondary inflammation of the eye
Facial ‘fullness’ and tenderness
Nasal discharge, pyrexia or post-nasal drip leading to cough
sinusitis
Management sinusitis
analgesia
if > 10 days - intranasal corticosteroids
severe : abx
Management medication overuse headache
simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
opioid analgesics should be gradually withdrawn
Management post lumbar puncture headache
Caffeine and fluids
if > 72 hours - may develop subdural haematoma - treat
Normal ICP
7-15 mmHg in adults in the supine position
A young, overweight woman is admitted to the medical assessment unit with headaches. Her CT head scan is normal, her lumbar puncture has an opening pressure of 30 cmH2O (reference range 5-25 cmH2O) and papilloedema is found on fundoscopy
IIH
Management IIH
- Weight loss
- acetazolamide (decreases fluid production)
- Topiramate
- Repeated lumbar puncture
- Surgery : optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.
- A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
Causes of obstructive hydrocephalus
tumours
acute haemorrhage (e.g. subarachnoid haemorrhage or intraventricular haemorrhage)
developmental abnormalities (e.g. aqueduct stenosis
Investigations for raised ICP
CT head is used as a first line imaging investigation since it is fast and shows adequate resolution of the brain and ventricles
MRI may be used to investigate hydrocephalus in more detail, particularly if there is a suspected underlying lesion
Lumbar puncture for non-obstructive hydrocephalus is both diagnostic and therapeutic since it allows you to sample CSF, measure the opening pressure, but also to drain CSF to reduce the pressure
selegiline, rasagiline
MAO-B
parkinsons management
Parkinsonism
Autonomic disturbance : erectile dysfunction often early feature, postural hypotension, atonic bladder
Cerebellar signs eg ataxia
multi-system atrophy
MSA-P - Predominant Parkinsonian features
MSA-C - Predominant Cerebellar features
Parkinsonism: bradykinesia prominent
Postural instability and falls
Stiff, broad-based gait
Impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficulty reading or descending stairs)
Cognitive impairment, primarily frontal lobe dysfunction
Supranucelar palsy / steele-richardson-olszewski syndrome
poor response to l-dopa
Urinary incontinence
Gait abnormality (shuffling and freezing)
Dementia and bradyphrenia (slowness of thought)
Normal pressure hydrocephalus
ventriculoperitoneal shunting (VP shunt)
progressive cognitive impairment (early impairments in attention and executive function rather than just memory loss)
cognition may be fluctuating, in contrast to other forms of dementia
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
later develops parkinsonism
Lewy body dementia
SPECT/DaTSCAN
Both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s
Neuroleptics are contraindicated
May use levodopa for parkinsonism
A 19-year-old man is referred to the general medical clinic. For the past six months his family have noted increasing behavioural and speech problems. He himself has noticed that he is more clumsy than normal and reports excessive salivation. His older brother died of liver disease.
disease
inheritance
investigations
management
Wilsons disease
autosomal recessive
Defect in ATP7B gene located on chromosome 13
Excessive copper deposition in the tissues (increased copper absorption from SI and decreased hepatic copper excretion
Investigations:
- Slit lamp examination for Kayser-Fleischer rings
- Increased 24hr urinary copper excretion
- Reduced serum ceruloplasmin
- Reduced total serum copper
- Free serum copper is increased
Diagnostic : genetic analysis of ATP7B gene
Penicillamine (chelates copper)
Management parkinsons
Motor symptoms affecting quality of life:
1. levodopa
Motor symptoms not affecting quality of life:
1. dopamine agonists, levodopa or monoamine oxidase B (MAO‑B) inhibitors
Do not offer ergot-derived dopamine agonists as first-line treatment for Parkinson’s disease
Name non-ergot dopamine agnoists
pramipexole, ropinirole, rotigotine and apomorphine
Name ergot dopamina agonists
what are ergot side effects
bromocriptine, pergolide, cabergoline
require monitoring due to fibrosis SE
adverse effects dopamine agonists
more adverse events eg Impulse control disorders
Excessive sleepiness and sudden onset of sleep
Psychotic symptoms
When to consider ergot-derived dopamine agnoists
in people who have developed dyskinesia or motor fluctuations despite optimal levodopa therapy and
in people whose symptoms are not adequately controlled with a non-ergot-derived dopamine agonist. [2017]
Management dyskinesia parkinsons
- modify meds
- amantadine
Management of generalised tonic-clonic seizures?
males: sodium valproate
females: lamotrigine or levetiracetam
girls aged under 10 years and who are unlikely to need treatment when they are old enough to have children or women who are unable to have children may be offered sodium valproate first-line
Management focal seizures?
first line: lamotrigine or levetiracetam
second line: carbamazepine, oxcarbazepine or zonisamide
Management of absence seizures?
first line: ethosuximide
second line:
male: sodium valproate
female: lamotrigine or levetiracetam
carbamazepine may exacerbate absence seizures
Management atonic/tonic seizures?
males: sodium valproate
females: lamotrigine
What epilepsy syndrome benefits from ketogenic diet?
Lennox-Gastaut syndrome
Management juvenile myoclonic epilepsy/ myoclonic epilepsy
males: sodium valproate
females: levetiracetam
Management infantile spasms (west syndrome)
- Prednisolone or Vigabatrin
vigabatrin - inhibiting the GABA-degrading enzyme, GABA transaminase, resulting in a widespread increase in GABA concentrations in the brain.
brachial plexus nerve roots
3 musketeers = musculocutaneous nerve C5, C6, C7
2 were assassinated = axillary nerve C5, C6 (gun sign with thumb and finger)
4 men (4 fingers) = median nerve C6, C7, C8, T1
5 rats = radial nerve C5, C6, C7, C8, T1
2 unicorns = ulnar nerve C8, T1
low back pain
bilateral sciatica
present in around 50% of cases
reduced sensation/pins-and-needles in the perianal area
decreased anal tone
it is good practice to check anal tone in patients with new-onset back pain
however, studies show this has poor sensitivity and specificity for CES
urinary dysfunction
e.g. incontinence, reduced awareness of bladder filling, loss of urge to void
incontinence is a late sign that may indicate irreversible damage
cauda equine
Investigation and management cuada equina
urgent MRI
surgical decompression
MRI finding normal pressure hydrocephalus
Ventriculomegaly without sulcal enlargement
What factors favour a true epileptic seizure over a psuedoseizure
tongue biting
raised serum prolactin
Investigations guilian barre
lumbar puncture
rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
nerve conduction studies may be performed
decreased motor nerve conduction velocity (due to demyelination)
prolonged distal motor latency
increased F wave latency
wasting in his calf muscles and high arches in his feet
charcot-marie tooth
Management guilian barre
IV immunoglobulins or plasma exchange
VTE prophylaxis (pulmonary embolism is a leading cause of death)
Symptoms of motor loss polyneuropathy
Ascending weakness
“Tripping over feet”
Foot drop
Hyporeflexia
Causes of motor loss polyneuropathy
Guillain-Barre syndrome
porphyria
lead poisoning
hereditary sensorimotor neuropathies (HSMN) - Charcot-Marie-Tooth
chronic inflammatory demyelinating polyneuropathy (CIDP)
Diphtheria
Pathophysiology charcot-marie tooth
CMT is caused by mutations in genes that support or produce proteins involved in the structure and function of either the peripheral nerve axon or the myelin sheath.
Because longer nerves are affected first, symptoms usually begin in the feet and lower legs and then can affect the fingers, hands, and arms.
The majority of mutations are inherited in an autosomal dominant pattern.
Investigations charcot-marie tooth
Diagnosis is made with a combination of nerve conduction studies and genetic testing. Patients with type 1 have reduced conduction velocity, whereas this is normal in type 2.
Abdominal pain, peripheral neuropathy motor, blue lines on gum margin
lead posioning
Causes of sensory polyneuropathy
A – Alcohol
B – B12 deficiency
C – Cancer and Chronic Kidney Disease
D – Diabetes and Drugs (e.g. amiodarone, metronidazole, cisplatin, phenytoin, isoniazid, nitrofurantoin, vincrystine)
E – Every vasculitis
Management of neuropathic pain
- amitriptyline, duloxetine, gabapentin or pregabalin
- if the first-line drug treatment does not work try one of the other 3 drugs
tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
pain management clinics may be useful in patients with resistant problems
Presentation of diabetic polyneuropathy
Distal Symmetrical Sensory Neuropathy
Most common
Caused by loss of large sensory fibres.
Sensory loss in a glove and stocking distribution.
Often affecting touch, vibration and proprioception.
Small-fibre Predominant Neuropathy
Caused by loss of small sensory fibres.
Presents with deficits in pain and temperature sensation in a glove and stocking distribution along with episodes of burning pain.
Autonomic neuropathy in diabetes
Presents with postural hypotension, gastroparesis, constipation, urinary retention, arrhythmias and erectile dysfunction.
Gastroparesis:
symptoms include erratic blood glucose control, bloating and vomiting
management options include metoclopramide, domperidone or erythromycin (prokinetic agents)
Presentation sensory polyneuropathy
Sensory symptoms:
Large fibre (dorsal column): touch, vibration, joint position (proprioceptive ataxia), painless paraesthesia
Small fibre (spinothalamic) : pain, temperature, burning, allodynia, hyperalgesia
Sensory ataxia affects patients with significant proprioceptive loss. Characteristically, the patient looks down and walks as if throwing his feet, which tend to slap on the ground. Smooth, familiar routes cause less trouble than uneven, rough ones.
allodynia and hyperalgesia definitons?
allodynia: pain due to a stimulus that does not normally provoke pain
hyperalgesia: increased sensitivity to pain
Diagnosing MS
two or more episodes disseminated in time and place (mcdonald criteria)
MRI with contrast
Categories of symptoms MS
Visual
Sensory
Motor
Cerebellar
Other
Visual symptoms MS
optic neuritis: common presenting feature (inflammation of the optic nerve causing sudden vision loss, colour blindness especially of the colour red and retrobulbar pain)
optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature
internuclear ophthalmoplegia (impaired lateral gaze due to damage to the medial longitudinal fasciitis) (nystagmus)
Sensory symptoms MS
pins/needles
numbness
trigeminal neuralgia
Lhermitte’s syndrome: paresthesia in limbs on neck flexion
Motor symptoms MS
spastic weakness: most commonly seen in the legs
Cerebellar symptoms MS
ataxia: more often seen during an acute relapse than as a presenting symptom
Tremor
Coordination of movement “off balance” “feels like world it moving”
Types of MS
Relapsing-remitting: relapse then complete resolution
Secondary progressive: relapses and remission but with ongoing deficit
Primary progressive: progressive, no remission from onset
Invetsigations MS
MRI (with contrast) periventricualar white plaques
Lesions disseminated in space and time
Oligoclonal bands in CSF
Management acute relapse of MS
High dose steroids (eg oral or IV methylprednisolone) for 5 days
Steroids shorten the duration of a relapse but don’t alter the degree of recovery
Disease modifying drugs MS
Natalizumab (a recombinant monoclonal antibody)
Fingolimod
beta interferon
glatiramer
Treatment of spasticity MS
Baclofen and gabapentin
Sudden vision loss, colour blindness especially of the colour red and retrobulbar pain
optic neuritis
What is internuclear opthalmaplegia
Internuclear ophthalmoplegia or ophthalmoparesis (INO) is an ocular movement disorder that presents as an inability to perform conjugate lateral gaze and ophthalmoplegia due to damage to the interneuron (medial longitudinal fasciculus) between two nuclei of cranial nerves (CN) VI and CN III (internuclear)
inhertiance charcot-marie tooth
autosomal dominant
what drugs increase risk of iih
combined oral contraceptive pill
steroids
tetracyclines
vitamin A
lithium
How does motor neurone disease present?
fasciculations
the absence of sensory signs/symptoms*
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
Other features
doesn’t affect external ocular muscles
no cerebellar signs
weakness, changes to reflexess and tone, fasiculations, in the absence of pain…
lower motor neurone signs
Muscle atrophy
Flaccid paralysis
No plantar response
Absent tendon reflexes
Fasciculations (single muscle fibres of uninjured LMN stimulated)
Investiagtions motor neurone disease
The diagnosis of motor neuron disease is clinical, but nerve conduction studies will show normal motor conduction and can help exclude neuropathy. Electromyography shows a reduced number of action potentials with increased amplitude. MRI is usually performed to exclude the differential diagnosis of cervical cord compression and myelopathy
Amyotrophic lateral sclerosis presentation
typically LMN signs in arms and UMN signs in legs
Primary lateral sclerosis presentation
UMN signs only
Progressive muscular atrophy presentation
LMN signs only
affects distal muscles before proximal
carries best prognosis
Progressive bulbar palsy presentation
palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis
management motor neurone disease
Riluzole
prevents stimulation of glutamate receptors
used mainly in amyotrophic lateral sclerosis
prolongs life by about 3 months
Respiratory care
non-invasive ventilation (usually BIPAP) is used at night
studies have shown a survival benefit of around 7 months
When do you initiate anticoagulation for someone with a stroke and newly diagnosed AF
Anticoagulation should be commenced 14 days after an ischaemic stroke. Earlier anticoagulation may exacerbate any secondary haemorrhage.
treat with aspirin as normal
management status epilepticus
1 Buccal midazolam or PR dizepam (pre-hospital)/ IV lorazepam (hospital)
2 IV lorazepam
3 IV phenytoin (phenobarbital if already on regular phenytoin)
4 Rapid sequence induction of anaesthesia using thiopental sodium
cerebellar signs
D - Dysdiadochokinesia, Dysmetria (past-pointing), patients may appear ‘Drunk’
A - Ataxia (limb, truncal)
N - Nystamus (horizontal = ipsilateral hemisphere)
I - Intention tremour
S - Slurred staccato speech, Scanning dysarthria
H - Hypotonia
cranial nerves implicated in acoustic neuroma
Cranial nerve V (trigeminal) - V1 (opthalmic) afferent (corneal) - main one for corneal
Cranial nerve VII (facial) efferent (corneal) and facial palsy
Cranial nerve VIII (vestibulocochlear) vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
Presentation acoustic neuroma
Vertigo, hearing loss, tinnitus and an absent corneal reflex
Bilateral vestibular schwannomas
neurofibromatosis type 2
Investigation and management ?acoustic neuroma
- urgent referral to ENT
- MRI of the cerebellopontine angle - gadalidium enhanced scan
- audiogram
- surgery, radiotherapy or observation
features of tuberus scleorsis
Cutaneous features
depigmented ‘ash-leaf’ spots which fluoresce under UV light
roughened patches of skin over lumbar spine (Shagreen patches)
adenoma sebaceum (angiofibromas): butterfly distribution over nose
fibromata beneath nails (subungual fibromata)
café-au-lait spots* may be seen
Neurological features
developmental delay
epilepsy (infantile spasms or partial)
intellectual impairment
retinal hamartomas: dense white areas on retina (phakomata)
rhabdomyomas of the heart
gliomatous changes can occur in the brain lesions
polycystic kidneys, renal angiomyolipomata
lymphangioleiomyomatosis: multiple lung cysts
features of neurofibromatosis T1
Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules) in > 90%
Scoliosis
Pheochromocytomas
There must be at least 2 of the 7 features to indicate a diagnosis. You can remember this with the mnemonic CRABBING.
C – Café-au-lait spots (6 or more) measuring ≥ 5mm in children or ≥ 15mm in adults
R – Relative with NF1
A – Axillary or inguinal freckles
BB – Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules) (2 or more) are yellow brown spots on the iris
N – Neurofibromas (2 or more) or 1 plexiform neurofibroma
G – Glioma of the optic nerve
features of neurofibromatosis T2
Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas
antiemetic for someone with parkinsons
Domperidone
what is cushings reflex
Bradycardia and hypertension with a wide pulse pressure is the correct answer.
Cushing’s triad, compromised of widening pulse pressure, bradycardia and irregular breathing, is a late sign indicating impending brain herniation.
Systolic hypertension occurs as a reflex to maintain cerebral perfusion pressure in the presence of raised intracranial pressure.
what is a pontine haemorrhage
Pontine haemorrhage is a life-threatening condition. It often occurs as a complication secondary to chronic hypertension. Patients often present with reduces Glasgow coma score, quadriplegia, miosis, and absent horizontal eye movements.
essential tremor presentation
bilateral fine intention tremor
Pharmacological treatments essential tremor
Propranolol (a non-selective beta blocker)
Primidone (a barbiturate anti-epileptic medication)
DVLA first unprovoked/isolated seizure
6 months off if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG.
If these conditions are not met then this is increased to 12 months
DVLA patients with established epilepsy or those with multiple unprovoked seizures
may qualify for a driving licence if they have been free from any seizure for 12 months
if there have been no seizures for 5 years (with medication if necessary) a ’til 70 licence is usually restored
DVLA withdrawal of epilepsy medication
should not drive whilst anti-epilepsy medication is being withdrawn and for 6 months after the last dose
DVLA syncope
simple faint: no restriction
single episode, explained and treated: 4 weeks off
single episode, unexplained: 6 months off
two or more episodes: 12 months off
DVLA stroke/TIA
1 month off driving, may not need to inform DVLA if no residual neurological deficit
DVLA multiple TIAs over short period of time
3 months off driving and inform DVLA
DVLA after craniotomy
craniotomy e.g. For meningioma: 1 year off driving
pituitary tumour: craniotomy: 6 months; trans-sphenoidal surgery ‘can drive when there is no debarring residual impairment likely to affect safe driving’
DVLA narcolepsy/cataplexy
cease driving on diagnosis, can restart once ‘satisfactory control of symptoms’
DVLA chronic neuro conditions eg MS, MND
DVLA should be informed, complete PK1 form (application for driving licence holders state of health)
axillary nerve mononeuropathy
Normal function:Shoulder abduction (deltoid muscle), sensory to inferior region of the deltoid muscle
Damage: Humerus surgical neck fracture: usually by direct blow or falling on an outstretched hand
Result: flattened deltoid, loss of sensation over deltoid
Radial nerve mononeuropathy
Normal function: Extension (forearm, wrist, fingers, thumb), (back off sign) sensory to small area between the dorsal aspect of the 1st and 2nd metacarpals
Damage: Humeral midshaft fracture
Result: Extensors become paralysed → unopposed flexion of the wrist ‘wrist drop’
Median nerve mononeuropathy
Normal function: LOAF* muscles. Wrist flexion, finger flexion, thumb opposition, pronation. (power to the people and okay sign, whip watch me okay) Sensory to Palmar aspect of lateral 3½ fingers
Damage: carpal tunnel syndrome, thenar wasting
Ulnar nerve mononeuropathy
Normal function: finger abduction and adduction. (peace sign) Sensory to Medial 1½ fingers
Damage: cubital tunnel syndrome/Supracondylar fracture/tardy ulnar palsy
how does hyperventilation to reduce icp work?
Hyperventilation -> reduce CO2 -> vasoconstriction of the cerebral arteries -> reduced ICP
Types of cerebral palsy
spastic (70%)
subtypes include hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons
dyskinetic
caused by damage to the basal ganglia and the substantia nigra
athetoid movements and oro-motor problems and dystonia
ataxic
caused by damage to the cerebellum with typical cerebellar signs
mixed
Myasthenia gravis associations
thymomas 15%
autoimmune conditions
Diagnostic investigation myasthenia gravis
Specific antibodies against the acetylcholine receptors AChR antibodies
If negative test anti-muscle-specific tyrosine kinase antibodies
single fibre electromyography: high sensitivity (92-100%)
CT thorax to exclude thymoma
CK normal
Mnagement myasthenia gravis
long-acting acetylcholinesterase inhibitors:
pyridostigmine is first-line
immunosuppression is usually not started at diagnosis, but the majority of patients eventually require it:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
thymectomy
Management of a myasthenic crisis
plasmapheresis
intravenous immunoglobulins
Plasmapheresis removes circulating antibodies, including the autoimmune antibodies responsible for the disease. Immunotherapy with intravenous gammaglobulin appears to diminish the activity of the disease.
MG implications for anaesthesia?
Suxamethonium is a depolarising NMBD - it acts by binding to and activating the receptor, at first causing muscle contraction, then paralysis. Due to a decreased number of available receptors, MG patients are typically resistant to depolarising NMBDs and may require significantly higher doses.
What drugs should be avoided in MG?
beta blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines
What is Lambert-Eaton ?
Progressive muscle weakness with increased use due to damage off NMJ. Asosociated with small cell lung cancer. Antibody against cancer attacks NMJ
Presentation lambert eaton
Insidious onset
proximal muscle weakness
Ptosis
Swallowing difficulties
Autonomic disturbance
Management lambert eaton
Amifampridine
Examination carpal tunnel syndrome
weakness of thumb abduction (abductor pollicis brevis)
wasting of thenar eminence (NOT hypothenar)
Tinel’s sign: tapping causes paraesthesia
Phalen’s sign: flexion of wrist causes symptoms
Management carpal tunnel syndrome
6-week cons if the symptoms are mild-moderate:
1. corticosteroid injection
2. wrist splints at night
Severe symptoms/persistent:
- surgical decompression (flexor retinaculum division)
what is frommets sign
Assess for ulnar nerve palsy
Adductor pollicis muscle function tested
Hold a piece of paper between their thumb and index finger. The object is then pulled away. If ulnar nerve palsy, unable to hold the paper and will flex the flexor pollicis longus to compensate (flexion of thumb at interphalangeal joint).
Management cubital tunnel syndrome
Avoid aggravating activity
Physiotherapy
Steroid injections
Surgery in resistant cases
Symptoms brain abscess
Headache
Fever
focal neurology
At what level does spinal lesion cause autonomic disturbance
at or above T6
UMN lesion
faecal impactation – urine retention – facial flushed etc
hypotension and tachycardia
what is hoovers sign
Hoover’s sign of leg paresis is a specific manoeuvre used to distinguish between an organic and non-organic paresis of a particular leg. This is based on the concept of synergistic contraction. If a patient is genuinely making an effort, the examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the ‘normal’ limb pushing downwards as the patient tries to raise their ‘weak’ leg, then this is suggestive of an underlying functional weakness, also known as ‘conversion disorder’.
Presentation cavernous sinus/venous sinus thrombosis
Headache – classically acute onset, often unilateral, with photophobia
Ophthalmoplegia and/or diplopia
Due to lesions on nerves of eye movements (CN 3, CN 4, CN 6)
Usually unilaterally, later progressing to both eyes
Causes cavernous sinus/venous sinus trombosis
local infection (e.g. sinusitis), neoplasia, trauma, prothrombotic states
What runs within cavernous sinus
Internal carotid arteries
Nerves –
CN 3 (oculomotor nerve)
CN 4 (trochlear nerve)
CN 5a & 5b (ophthalmic and maxillary branches of trigeminal nerves)
CN 6 (abducens nerve)
Post-ganglionic sympathetic nerve fibres
Investigations venous thromboses
MRI venography is the gold standard
CT venography is an alternative
non-contrast CT head is normal in around 70% of patients
D-dimer levels may be elevated
Presentation saggital sinus thrombosis
Seizures and hemiplegia
parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
‘empty delta sign’ seen on venography
Most common cancer to metastise to brain
Lung (most common)
Breast
Renal cell carcinoma
Melanoma
Bowel
Kidney
What are glial cells
provide support and nutrients for neurones
what are gliomas
tumours of glial cells
Most common priamary brain tumour in adults
glioblastoma multiforme / grade IV astrocytoma
Most malignant glioma
glioblastoma multiforme / grade IV astrocytoma
glioblastomaon imaging and histology
solid tumours with central necrosis and a rim that enhances with contrast
Pleomorphic tumour cells border necrotic areas
Management of glioblastoma
Treatment is surgical with postoperative chemotherapy and/or radiotherapy. Dexamethasone is used to treat oedema.
imaging and histology meningioma
CT
* Histology: Spindle cells in concentric whorls and calcified psammoma bodies
* Investigation is with CT (will show contrast enhancement) and MRI
location meningiomas
falx cerebri, superior sagittal sinus, convexity or skull base
Cause of huntingtons
more than 38 repeats of the CAG trinucleotide
Prevalence huntingtons
between 1 in 10,000 and 1 in 20,000.
Scan huntingtons
MRI and CT scans in moderate to severe disease can show loss of striatal volume and increased size of the frontal horns of the lateral ventricles. (MRI shows atrophy of the caudate nucleus and putamen)
Diagnosis huntingtons
genetic testing
Management chorea
tetrabenazine
What level controls diaphragm
C4 level,
Where do meningiomas arise from?
arachnoid cap cells of the meninges and are typically located next to the dura
Symptoms meningiomas
Cause symptoms by compression rather than invasion
Changes in vision, such as seeing double or blurriness.
Headaches, especially those that are worse in the morning.
Hearing loss or ringing in the ears.
Memory loss.
Loss of smell.
Seizures.
Weakness in your arms or legs.
Histology acoustic neuroma
Antoni A or B patterns are seen. Verocay bodies (acellular areas surrounded by nuclear palisades)
Most common primary brain tumour in children?
Histology?
Pilocytic astrocytoma
Rosenthal fibres (corkscrew eosinophilic bundle)
How do patients with pituitary adenoma present?
Patients will present with the consequences of hormone excess (e.g. Cushing’s due to ACTH, or acromegaly due to GH) or depletion. Compression of the optic chiasm will cause a bitemporal hemianopia due to the crossing nasal fibers.
What is cushings syndrome
excess ACTH –> excess cortisol
Most common paediatric supratentorial tumour? how does it present?
Craniopharyngioma
hormonal disturbance, symptoms of hydrocephalus or bitemporal hemianopia.
Where does craniopharyngioma originate from?
Derived from remnants of Rathke pouch
Investigations and treatment craniopharyngioma
Investigation requires pituitary blood profile and MRI. Treatment is typically surgical with or without postoperative radiotherapy.
What are the features of Creutzfeldt-Jakob disease
dementia (rapid onset)
myoclonus
MRI creutzfeldt-Jakob disease
hyperintense signals in the basal ganglia and thalamus.
EEG creutzfeldt-Jakob disease
biphasic, high amplitude sharp waves
CSF creutzfeldt-JAkob disease
normal
What protein is responsible for creutzfeldt jakob disease
prion proteins
Define dystonia
prolonged, often painful, muscle contraction
PResentation Polymyositis/dermatomyositis
proximal muscle weakness +/- tenderness
Raynaud’s
respiratory muscle weakness
interstitial lung disease: e.g. fibrosing alveolitis or organising pneumonia
dysphagia, dysphonia
dermatomyositis is a variant of the disease with skin manifestations eg a purple (heliotrope) rash on the cheeks and eyelids
First line invetsigation polymyositis/dermatomyositis
elevated creatine kinase
Definitive diagnosis polymositis/dermatomyositis
msucle biopsy
Pathophysiology polymyositis/dermatomyositis
thought to be a T-cell mediated cytotoxic process directed against muscle fibres
may be idiopathic or associated with connective tissue disorders
associated with malignancy
Management polymyositis/dermatomyositis
- corticosteroids
- additional immunosuppressant such as methotrexate or azathioprine as a steroid-sparing agent.
- hydroxycloriquine for dermatomyositis
What drugs can cause myopathy
chronic corticosteroids (CK normal)
acute corticosteroids (CK raised)
statins (CK raised)
triad rhabdomyolysis
dark urine, generalised weakness and myalgia
dianostic rhabdomyolysis
CK > 5x normal. this can then cause aki
MAnagement rhabdomyolysis
IV fluids to maintain good urine output
urinary alkalinization (eg sodium bicarbonate) is sometimes used
management of electrolyte imbalance such as potassium
Electrolyte changes rhabdomyolysis
Raised LDH (suggestive of muscle damage)
Hyperkalaemia (liberated from the damaged muscle) (aki)
Hyperphosphatemia (liberated from the damaged muscle)
Hyperuricaemia (liberated from damaged muscle)
Hypocalcaemia (calcium is taken into the damaged muscle by several mechanisms)
What drug is co-prescribed with levodopa to prevent side effects
Dopa decarboxylase inhibitor (e.g. carbidopa or benserazide)
side effects levodopa
- hallucinations
- dyskinesia
- postural hypotension on starting
- on/off effect
- dry mouth
- palpitations
Where is the damage in dyskinetic cerebral palsy
results from damage to the basal ganglia and the substantia nigra
Klumpke’s paralysis
damage to T1
Spasticity vs rigidity
Spasticity occurs in pyramidal tract lesions and is due to 1. Increased activity of alpha motor neurons and it is velocity dependent
eg. clasp knife and ankle clonus
Rigidity occurs in extrapyramidal lesions and is due to increased activity of gamma neurons 2. Not velocity dependent. eg cogwheel and lead pipe
flow of cerebrospinal fluid
- Lateral ventricles (via foramen of Munro)
- 3rd ventricle
- Cerebral aqueduct (aqueduct of Sylvius)
- 4th ventricle (via foramina of Magendie and Luschka)
- Subarachnoid space
- Reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus
BAmford classification total anterior circualtion stroke
All three of the following need to be present for a diagnosis of a TACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg (at least 2/3)
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)
Bamford classification partial anterior cirucaltion stroke
Two of the following need to be present for a diagnosis of a PACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)*
*Higher cerebral dysfunction alone is also classified as PACS.
Bamford classification posterior ciruclation stroke
One of the following need to be present for a diagnosis of a POCS:
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia
Bamford classification lacunar stroke
One of the following needs to be present for a diagnosis of a LACS:
Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis
cause of anterior cord syndrome
ischemia within the anterior spinal artery (ASA)
Adverse effects sodium valproate
-alopecia
-hepatitis
-pancreatitis
-thrombocytopenia
-teratogenic
-Increased appetite and weight gain
-P450 enzyme inhibitor
-ataxia
-tremor
Adverse effects carbmazepine
-leucopenia and agranulocytosis
P450 enzyme inducer
-dizziness and ataxia
-drowsiness
-inappropriate ADH secretion
-visual disturbances (diplopia)
Adverse effects lamorigine
-stevens-johnson syndrome
Adverse effcects phenyoin
-megaloblastic anaemia
-p450 enzyme inducer
-dizziness and ataxia
-drowsiness
Gingival hyperplasia, hirsutism, coarsening of facial features
-peripheral neuropathy
-enhanced vitamin D metabolism causing osetomalacia
-lymphadenopathy
Process of invetsgigating SAH
- CT head non-contrast (may show star sign)
- Lumbar puncture (xnathachromia)
- CT angiography (gold standard - shows where lesion is)
Adverse effects ethosuximide
night terrors
In a SAH, what artery would be implicated if they had a occulomotor nerve palsy
posterior cmmunicating artery
Dysphasia vs dysarthria
dysphasia - language problem eg brocas
dysarthria - muscle impairment meaning can’t create sound properly
what is tardy ulnar palsy
damage to ulnar nerve at the wrist –> unopposed action of upper undamaged ulnar –> flexion of 4th and 5th digits (claw hand)
cuases of common peroneal nerve palsy
posturing eg crossing legs
fracture of neck of fibula
what is tarsal tunnel syndrome
damage to tibial nerve - pain numbness and tingling in feet
medial malleous
How to ddx peroneal nerve palsy from L5 radiculopathy
L5 radiculopathy also has issues with hip abduction and foot inverson
whcih radiculopathies are femoral stretch test positive
L3 and L4
what is ROSIER
ROSIER is a clinical scoring tool based on clinical features and duration. Stroke is likely if the patient scores anything above 0.
Secondary prevention stroke
Anti-platelet:
1. clopidogrel 75 mg daily.
2. Aspirin 75 mg daily with modified-release dipyridamole 200 mg twice daily
3. Modified-release dipyridamole 200 mg twice daily
Statin 80mg
Antihypertensive if required
Anticoagulation after 14 days if indicated eg AF
what is keppra
brand name for levetiracetam
examples of decarboxylase inhibitors
Cobeneledopa = levodopa + benserazide
Cocareldopa = levodopa + carbidopa
MRI exam buzzword: hot cross bun sign
multiple systems atrphy
MRI exam buzzword: hummingbird sign
progressive supranucelar palsy
do CN lesions cause contralateral or ipisilateral symptoms?
all ipsilateral apart from trochlear (4th)
Which CN at midbrain?
3 and 4
Which CN at pons
5, 6, 7, 8
Which CN at medulla
9,10, 11, 12
BP contraindication for thrombolysis
180/110mmHg is a contraindication for thrombolysis.
Arnold-Chiari malformation
Arnold-Chiari malformation describes the downward displacement, or herniation, of the cerebellar tonsils through the foramen magnum. Malformations may be congenital or acquired through trauma.
Features
non-communicating hydrocephalus may develop as a result of obstruction of cerebrospinal fluid (CSF) outflow
headache
syringomyelia
triad parkinsons
tremor, rigidity, and bradykinesia
what is a colles fracture? what erve can be damaged?
Colles’ fracture – The most common type of radial fracture. A fall onto an outstretched hand causing a fracture of the distal radius. The structures distal to the fracture (wrist and hand) are displaced posteriorly. It produces what is known as the ‘dinner fork deformity’.
median eg can’t abduct thumb
when is carotid endarterectomy indicated?
Carotid endarterectomy is considered in a patient who has had a TIA with carotid artery stenosis exceeding 70%
neuro incontinence vs retention?
UMN - urinary retention as hypertonic sphincters
LMN - urinary incontinence as hypotonic sphincters
