Neurology Flashcards
Give 3 primary headaches
-Migraine
-Cluster
-TensionF
Give 8 typical features of a migraine
-Last 4 to 72 hours
-Unilateral
-Pounding/throbbing in nature
-Moderate to severe intensity
-Photophobia
-Phonophobia
-With or without aura
-N&V
Give the 5 stages of a typical migraine
-Prodromal stage -> up to 3 days before headache
-Aura -> up to 60mins
-Headache
-Resolution
-Postdromal/recovery phase
Give 8 possible triggers for a migraine
-Stress
-Bright lights
-Strong smells
-Certain foods (chocolate, cheese, caffeine)
-Dehydration
-Menstruation
-Abnormal sleep patterns
-Trauma
What is aura ?
-Visual changes associated with a migraine
-Can be : sparks in vision, blurring vision, lines across visions and loss of different visual fields
How is a migraine acutely managed ?
-Paracetamol, NSAIDs
-Triptans (e.g sumatriptan, 50mg as the migraine starts)
-Antiemetic
What kind of medication is a triptan ?
-5HT receptor agonists (serotonin receptor agonists)
What do triptans act on?
-Smoot muscle in arteries causing vasoconstriction
-Peripheral pain receptors to inhibit their activation
-Reduce neuronal activity in the CNS
What can be used for migraine prophylaxis ?
1st : Propranolol and Topiramate -> teratogenic.
-Amitriptyline
-Acupuncture
What can be used to reduce the frequency and severity of migraines?
-Vitamin B2 (Riboflavin)
What can be used for prophylaxis with migraines associated with menstruation ?
-NSAIDs (e.g. mefanamic acid)
-Triptans (frovatriptan, zolmitriptan)
What is a cluster headache ?
-Severe and unbearable unilateral headache, typically around the eye.
-Lasts 15 mins to 2 hrs
Explain the pattern of occurrence of cluster headaches
-Clusters of attacks before disappearing for a while
-E.g 3-4 attacks a day for a week/mnth followed by a pain-free period lasting 1-2 years
What can trigger cluster headaches?
-Alcohol
-Strong smells
-Exercise
Give 5 symptoms of a cluster headache
-Red, swollen and watering eye
-Pupil constriction (miosis)
-Eyelid dropping (ptosis)
-Nasal discharge
-Facial sweating
How is a cluster headache managed acutely ?
-Triptan (e.g. sumatriptan 6mg injected subcut)
-High flow 100% oxygen for 15-20 mins
Give 3 prophylactic options for a cluster headache
-Verapamil (CCB)
-Lithium
-Prednisolone (short course for 2-3 wks to break the cycle during clusters)
What is a tension headache ?
-Mild headache across the forehead in a band-like pattern around the head
- Lasts mins - days
Give 5 associations of a tension headache
-Stress
-Depression
-Alcohol
-Skipping meals
-Dehydration
Give 2 treatment options for a tension headache
-Reassurance
-Basic analgesia
Explain sinusitis
-Inflammation in the ethmoidal, maxillary, frontal or sphenoidal sinuses can cause a headache
-Usually produces facial pain behind the nose, forehead and eyes (worse on bending forward)
-Often tenderness over affected sinus
- Nasal discharge
- Nasal onstruction
What is an analgesic headache
-Headache caused by long term analgesia
-Presents similar to a tension headache
What is cervical spondylosis ?
-Common condition caused by degenerative changes in the cervical spine (OA)
-Causes neck pain worse on movement but can also present with a headache
How does trigeminal neuarlgia present ?
-Intense facial pain
-Described as electricity-like shooting pain
-90% unilateral
What can trigger trigeminal neuralgia and what is a common association
-Triggers : cold weather, spicy food, caffeine and citrus fruit
-5 to 10% of ppl with MS have trigeminal neuralgia
how is trigeminal neuralgia treated ?
-1st line -> carbamazapine
-Surgery to decompress or intentionally damage the nerve
Give the 3 branches of the trigeminal nerve
-Opthalmic (V1)
-Maxillary (V2)
-Mandibular (V3)
Give 4 causes of an ischaemic stroke
-Embolism : embolus from somewhere else in the body
-Thrombosis : blood clot forming locally with in the vessel
-Systemic hypoperfusion (e.g. cardiac arrest)
-Cerebral venous sinus thrombosis : blood clot in veins that drain the brian
Explain the blood supply to the cerebrum
-Anteromedial cerebrum : anterior cerebral artery
-Lateral cerebrum : middle cerebral artery
-Posterior cerebrum : posterior cerebral arteries
what classifies as a partial anterior circulation stroke (PACS)?
-TWO of the following :
-Unilateral weakness or sensory disturbance
-Homonymous hemianopia
-Higher cerebal dysfunction (dysphagia, visuospatial disorder)
What classifies as a total anterior circulation stroke (TACS)
-BOTH the middle and anterior cerebral arteries affected.
-THREE of the following :
-Unilateral weakness or sensory disturbance
-Homonymous hemianopia
-High cerebral dysfunction
Posterior cerebral artery stroke
- Contralateral homonymous hemianopia with macular sparing
- Visual agnosis
What has to be present for a diagnosis of a lacunar stroke?
ONE of the following needs to be present :
- Pure one-sided sensory loss
- Unilateral motor disturbance
- Ataxic hemiparesis
What is the immediate management of an ischaemic stroke ?
-Thrombolysis with alteplase if within 4.5 hrs
-300mg of aspirin and continue for 2 wks
-Thrombectomy if thrombolysis is CI
What is the longterm management for an ishcaemic stroke ?
-75mg of clopidogrel daily (+PPI)
-80mg atorvostatin but not immediately
-If pt has carotid stenosis -> consider carotid endarterectomy
What are the RF for a stroke (8)
-CVD
-Previous stroke or TIA
-AF
-Hypertension
-DM
-Smoking
-Vasculitis
-Combined contraceptive pill
Define MS
- Autoimmune demyelination of the CNS
What cells produce myelin in the CNS and in the PNS ?
-CNS : oligodendrocytes
-PNS : schwann
How do the episodes of demyelination present in MS?
-Episodes disseminated in time and space
What is optic neuritis ?
-Unilateral painful reduced vision developing over hrs to days.
Give 4 key features of optic neuritis
-Central scotoma (blind spot)
-Pain on eye movement
-Impaired colour vision
-Relative afferent pupillary defect
Give 7 other causes of optic neuritis other than MS
-Sarcoidosis
-SLE
-DM
-Syphilis
-Measles
-Mumps
-Lyme disease
What investigations can support a diagnosis of MS
- MRI -> lesions
- LP -> oligoclonal bans in CSF
- McDonald criteria for diagnosing
Give the 4 disease patterns of MS
-Clinically isolated syndrome
-Relapsing-Remitting
-Secondary progressive
-Primary progressive
Explain the relapsing-remitting pattern of MS
-Episodes of disease followed by recovery. Classified on whether active and/or worsening
-Active : new symptoms developing
-Not active : no new symptoms developing
-Worsening : overall worsening of disability over time
-Not worsening : no worsening of disability over time
Explain secondary progressive pattern of MS
-Was relapsing/remitting but now a progressive worsening of symptoms
-Can also be classified as active and/or worsening
Explain primary progressive pattern of MS
-Worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions
Give two common characteristics of MS
-Lhermitte’s sign : tingling electric shock shooting up the spine when flexing the neck
-Uhthoff’s phenomenon : symptoms are worse when hpt (e.g. in bath, hot weather, exercise).
What can be used to treat relapses in MS?
-Methylprednisolone
-500mg orally for 5 days or 1g IV for 3-5 days if treatment fails
What is the pathophysiology behind MND?
-Progressive degeneration of both upper and lower motor neurones
-Sensory neurones are spared
What can increase the risk of MND?
-Smoking
-Exposure to heavy metals
-Certain persticides
What is a typical presentation of MND
- Late middle aged man
- Insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech
- Weakness often first noticed in upper limbs
- Fatigue when exercising
Give 4 signs of lower MND
-Muscle wasting
-Reduced tone
-Fasciculations
-Reduced reflexes
GIve 3 signs of upper MND
-Increased tone or spasticity
-Brisk reflexes
-Upgoing plantar responses
What is the most common presentation of MND ?
-Amyotrophic lateral sclerosis (ALS)
- Typically LMN signs in the arms and UMN signs in the legs
What can be used to slow the progression of MND ?
-Riluzole
What is myasthenia Gravis ?
-Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest
- Affects the NMJ
What is strongly associated with myasthenia Gravis?
-Thyoma : tumour of the thymus gland
Explain the pathophysiology behind myasthenia gravis
-In most cases, acetylcholine receptor antibodies are produced
-These bind to the postsynaptic receptors
-This prevents the stimulation of the receptor and so prevents muscle contraction
-The antibodies also activate the complement system, leading to damage to the cells of the postsynaptic membrane further worsening the symptoms
Why do the symptoms of myasthenia gravis get worse with exercise ?
-The receptors are used more during muscle activity and so more of them become blocked up.
-This leads to less effective stimulation of the muscle with increased activity
-There is more muscle weakness the more the muscles are used
-This improves with rest as more receptors are freed up again for use
What are 2 other antibodies involved in myasthenia gravis?
-Muscle-specific kinase (MuSK)
-Low density lipoprotein receptor-related protein (LRP4)
-These proteins are imprtant for the creation of acetylcholine receptor
-Destruction of these by the antibodies leads to inadequate acetylcholine receptors
What is a characteristic feature of myasthenia gravis
-Weakness that gets worse with muscle use and improves with rest
What muscles are most affected in myasthenia gravis ?
-Proximal muscles and small muscles of the head and neck
Give 8 common symptoms of myasthenia gravis
- Diplopia : extraocular muscle weakness
- Ptosis
- Weak upwards gaze
- Weakness in facial movements
- Difficulty with swallowing
- Fatigue in the jaw when chewing
- Slurred speech
- Progressive weakness with repetitive movements
Give 3 things to assess of examination for myasthenia gravis
-Thymectomy scar
-FVC
-Elicit fatiguability of muscles : repeated blinking will exacerbate ptosis ; prolonged upward gaze with exacerbate diplopia ; repeated abduction of one arm 20 times with result in unilateral weaknes when comparing both sides
Give 3 investigations for diagnosing myasthenia gravis
- Test for antibodies
- CT/MRI of the thymus to check for thymoma
- Edrophonium test if in doubt (tensilon)
What is the edrophonium test
-Used to aid diagnosis of myasthenia gravis
What is the edrophonium test
-Used to aid diagnosis of myasthenia gravis
-IV edrophonium chloride is given which will prevent the breakdown of acetylcholine
-Acetycholine levels will rise giving temporary relief from the weakness
Give 3 treatment options for myasthenia gravis
-Pyridostigmine -> reversible acetylcholinesterase inhibitors -> increase the amount of acetylcholine at the junction (or rivastigmine)
-Immunosuppression with prednislone or azathioprine : suppress antibody production
-Thymectomy
What 2 monoclonal antibodies can be used in myasthenia gravis ?
-Rituximab -> targets b cells reducing antibody production
-Eculizumab -> targets complement protein C5.
What is a myasthenic crisis?
-Acute worsening of symptoms often triggered by a viral infection
-Can lead to resp failure due to weakness in the muscle of respiration
- FVC needs monitoring
What is used in the management of a myasthenic crisis?
- IV immunoglobulins
- Plasmapheresis
If needed :
- BiPAP
- Intubation and ventilation
What is Lambert-Eaton myasthenic syndrome ?
autoimmune condition affecting the neuromuscular junction
Who is usually affected by Lambert-Eaton myasthenic syndrome ?
-Patients with small cell lung cancer
Explain the pathophysiology behind Lambert-Eaton myasthenic syndrome
- Antibodies against voltage-gated calcium channels in the SCLC are produced.
- These target and damage the same channels in the presynaptic terminals of the neuromuscular junction
- This results in less acetylcholine being released into the synapse
How does lambert-eaton syndrome present ?
-Proximal muscles most affected -> leg muscle weakness (difficulty climbing stairs)
- Reduced or absent tendon reflexes
-Autonomic dysfunction : dry mouth, blurred vision, impotence and dizziness
-Double vision
-Ptosis
-Dysphagia
What is post-tetanic potentiation ?
-In lambert-eaton syndrome, tendon reflexes are normally reduced
-They can become temporarily normal for a short period following a period of strong muscle contraction
How is lambert-eaton syndrome managed?
-Treat underlying malignancy if present
-Amifampridine
-Immunosuppressants
-IV immunoglobulins
-Plasmaphersis
How does amifampridine work in the treatment of Lambert-Eaton?
-It blocks voltage-gated potassium channels in the presynaptic cells
-This prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action
Define Gullian-Barre syndrome (GBS)
-Acute paralytic polyneuropathy affecting the peripheral nervous system
What usually triggers GBS ?
-Infection
-Campylobacter jejuni (food poisoning), cytomegalovirus, EBV
How does GBS present ?
- Back/leg pain in initial stages
- Symmetrical ascending weakness
- Reduced reflexes
-+/- peripheral loss of sensation or neuropathic pain - May progress to cranial nerves and cause diplopia, bilateral facial nerve palsy and oropharyngeal weakness
What is the clinical course of GBS?
-Preceding infection
-Symptoms begin 4 wks later
-Symptoms peak after 2-4 wks
-Recovery period lasting mnths to years
What investigations support the diagnosis of GBS?
-Once clinically diagnosed using Brighton criteria :
-Nerve conduction studies showing reduced signal through the nerves
-LP : raised protein with normal cell count and glucose
How is GBS managed ?
- IV immunoglobulins
- Plasmapheresis can be an alternative to IVIG
- VTE prophylaxis with LMWH
What are the features of a benign essential tremor ? (6)
-Fine tremor
-Symmetrical
- 6-12 Hz
-MORE prominent on VOLUNTARY movement
-Worse when tired, stressed or after caffeine
-Improved by alcohol
-Absent during sleep
Give 6 differentials of a tremor
-Parkinson’s
-MS
-Huntington’s chorea
-Hyperthyroidism
-Fever
-Medications (e.g. antipsychotics)
What 2 medications can improve the symptoms of a benign essential tremor ?
-Propranolol
-Primidone
What is the cause of parkinson’s ?
- Progressive reduction of dopamine in the basal ganglia
- Leads to disorders of movement
- Symptoms are ASYMMETRICAL
What is the classic triad of parkinson’s
- Cogwheel rigidity
- Pill-rolling resting tremor (4-6Hz)
- Bradykinesia : smaller handwriting, shuffling gate, difficulty initiating movements, reduced facial expressions (hypomimia)
postural instability is an extra
Where is dopamine produced ?
-Substantia nigra of the basal ganglia
Give 5 other features of parkinson’s
-Depression
-Sleep disturbance and insomnia
-Anosmia
-Postural instability
-Cognitive impairment and memory problems
Describe a parkinson’s tremor
-Asymmetrical
-WORSE at REST
-IMPROVES with INTENTIONAL movement
-No change with alcohol
Give 4 treatment options for parkinson’s
- Co-benyldopa or co-careldopa
- COMT inhibitors
- Dopamine agonists
- Monoamine Oxidase-B Inhibitors
Explain how levodopa works
-Synthetic dopamine
-Most effective but becomes less effective over time
What is usually given with levodopa and why?
-Peripheral decarboxylase inhibitor
-Stops is being broken down before it reaches the brain
-Examples : carbidopa, benserazide
What is the main side effect of levodopa?
- Too high dopamine = dyskinesias = abnormal movements associated with excessive motor activity.
- E.g. dystonia, chorea, athetosis
How do COMT inhibitors work?
-Example : entacapone
-Inhibits catechol-o-methyltransferase which is responsible for metabolising levodopa
-Extends to duration of levodopa
How do dopamine agonists work ?
- Mimic dopamine in the basal ganglia and stimulate dopamine receptors
- Less effective than levodopa
- Examples : bromocryptine, pergolide, cabergoline
What is the most notable side effect of dopamine agonists with prolonged use ?
- Pulmonary fibrosis
How do monoamine Oxidase-B Inhibitors work?
-They block Monoamine Oxidase-B enzyme which is responsible for breaking down dopamine
-Examples are selegiline and rasagiline
Name 4 parkinson plug syndromes
- multiple system atrophy
- Dementia with lewy bodies
- progressive supranuclear palsy
- corticobasal degeneration
What is multiple system atrophy
- Neurones of multiple systems in the brain degenerate
What is dementia with lewy bodies
- Dementia w/ features of Parkinsonism
- Causes progressive cognitive decline
- Associated symptoms : visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness
- Anti-parkinson meds may worsen psychosis
Give 6 risk factors for an intracranial bleed
-Head injury
-HTN
-Aneurysm
-Brain tumour
-Anticoagulants
-Ishcaemic stroke progressing to haemorrhagic
How does an intracranial bleed present ?
-Sudden onset headache
-Seizures
-Weakness
-Vomiting
-Reduced consciousness
-Other sudden onset neurological symptoms
Explain a subdural haemorrhage
- RF : elderly, alcholics, anticoag, recent trauma
- Rupture of bridging veins between the dura and arachnoid
- Px : fluctuating conspicuousness, headache, drowsy, can be present for wks
- Ix : Crescent shaped on CT and do not cross suture lines. Chronic = dark/hypodense. Acute = bright/hyperdense
- Tx : burr hole craniotomy, stop anticoag and drainage, supportive mannitol
Explain an extradural haemorrhage
- Usual Rupture of middle meningeal artery in the temporal region
- Px : Traumatic head injury, LOC, lucid period, rapid decline in GCS, headache, N&V
- Ix : lentiform heterogenous hyper-dense extra-axial collection adjacent to temporal bone (lemon)
Explain an intracerebral haemorrhage
-Bleeding into the brain tissue
-Presents similar to an ischaemic stroke
Expain a subarachnoid haemorrhage
- Bleeding into the subarachnoid space between the pia and the arachnoid membrane
- Usually a result of berry aneurysm (also trauma and atrioventricular malformation)
How does a subarachnoid haemorrhage present ?
- Sudden onset occiptal headache : ‘thunderclap headache’
- Neck stuffness
- Photophobia
- Vision changes
- Neurological symptoms : speech changes, weakness, seizures and loss of consciousness
What are subarachnoid haemorrhages associated with (5)
-Cocaine use
-Sickle cell anaemia
-Connective tissue disorders
-Neurofibromatosis
-Autosomal dominant PKD
What is seen on a CT in a subarachnoid haemorrhage
-Hyperattenuation in the subarachnoid space (star shape)
What is seen on an LP in a subarachnoid haemorrhage
-Raised red cell count
-Xanthochromia (yellow colour of CSF caused by bilirubin after 12 hrs)
How can a subarchnoid haemorrhage be managed ?
-Coiling or clipping of the aneurysm
- Nimodipine (CCB) to prevent vasospasm
- LP or shunt insertion if hydropcephalus occurs
- Antiepileptics for seizures
Give 3 complications of a subarachnoid haemorrhage
-Vasospasm
-Hydrocephalus
-Seizures
What is Charcot-Marie-Tooth disease and what is the usual inheritance pattern?
- Hereditary motor and sensory neuropathy
- Autosomal dominant
Give 7 features of Charcot-Marie-Tooth ?
-High foot arches (pes cavus)
-Distal muscle wasting causing ‘inverted champagne bottle legs’
-Weakness in lower legs, particularly loss of ankle dorsifelxion (with high stepping gait due to foot drop)
-Weakness in the hands
-Reduced muscle tone
-Reduced tendon reflexes
-Peripheral sensory loss
Give 5 causes of peripheral neuropathy
-A : alcohol
-B : B12 deficiency
-C : cancer and chronic kidney disease
-D : diabetes and drugs (e.g isoniazid, amiodarone & cisplatin)
-E : every vasculitis
What is tuberous sclerosis ?
- Autosomal dominant condition affecting multiple systems, resulting in the development of hamartomas
What are hamartomas and where do they usually occur in tuberous sclerosis
-Benign neoplastic growths of the tissue
-Skin, brain, lungs, heart, kidneys and eyes
What causes tuberous sclerosis ?
-> Mutations in one of two genes
-> TSC1 on chromosome 9 -> hamartin
-> TSC2 on chromosome 16 -> tuberin
-> Hamartin and tuberin interact with each other to control the size and growth of the cells
-Abnormalities in these lead to abnormal cell size and growth
Give 2 neurological features of tuberous sclerosis
-Epilepsy
-Learning disability and developmental delay
Give 3 skin signs of tuberous sclerosis
-Ash leaf spots : depigemented areas of skin shaped like ash leaf
-Angiofibromas : papules on nose and cheeks
-Poliosis : white patch of hair on head, eyebrows, eyelashes or beard
What is the preffered way to support nutrition in patients with MND?
-Percutaneous gastrostomy tube
What is a pontine haemorrhage ?
-Life threatening condition occurring secondary to chronic hypertension
-Patients present with reduced GCS, quadriplegia, miosis and absent horizontal eye movements
What classes as a lacunar infarct?
-ONE of the following :
-Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three
-Pure sensory stroke
-Ataxic hemiparesis : weakness and impaired co-ordination on one side
-Involves perforating arteries around the internal capsule, thalamus and basal ganglia
What is Bell’s palsy ?
- Acute, unilateral, idiopathic, lower motor neuron facial nerve palsy -> FOREHEAD AFFECTED
- Lower motor neuron facial nerve palsy affecting the forehead
- Possible pain, altered taste, dry eyes and hyperacusis (everyday sounds seem much louder)
How is Bell’s palsy managed ?
- Oral prenisolone within 72 hrs of onset (50mg for 10 days, 60mg for 5 days, followed by 5-day reducing regime of 10mg)
- Eye care -> eye lubricants, tape closed at night with microporous tape
- Return to ENT if no improvement within 3 weeks
What is a complication of Bell’s palsy ?
-Exposure keratopathy : dry and damaged eye
What is neurofibromatosis ?
-Genetic condition causing nerve tumours (neuromas)
-Neurofibromatosis type 1 is more common than type 2
-Usually autosomal dominant inheritance
What is the the role of the neurofibromatosis type 1 gene ?
-Codes for neurofibromin -> a tumour suppressor protein
-Found on chromosome 17
What are the diagnostic features for neurofibromatosis type 1 ?
-2 of the following :
-CRABBING
-C : Cafe-au-lait spots (>6)
-R : Relative with NF1
-A : Axillary or inguinal freckles
-BB : Bony displasia such as Bowing of a long bone or sphenoid wing displasia
-Iris hamartomas (Lisch nodules)
-Neurofibromas (>2) or 1 plexiform neurofibroma
-G : Glioma of the optic nerve
What is the role of the neurofibromatosis type 2 gene ?
-Codes for merlin -> a tumour suppressor gene important in Schwann cells
-Chromosome 22
-Mutations lead to schwannomas
What is a generalised tonic-clonic seizure?
- Loss of consciousness with muscle tensing
- Followed by clonic phase of muscle jerking
- Associated tongue biting, incontinence, groaning and irregular breathing
- Post-ictal period : confusion, drowsy, irritable and depressed
How are tonic-clonic seizures managed ?
- 1st line : sodium valporate
- 1st line in females = levetiracetam
What are focal seizures
- Begin in a certain part of the brain (e.g. temporal lobes)
-If in temporal lobe can affect hearing, speech, memories and emotions - May present with hallucinations, memory flashbacks, deja vu
- 1st line : carbamazapine or lamotrigine
- 2nd line : sodium valporate
What are absence seizures
- Usually occurs in children (3-10, F>M)
- Pt becomes blank and stares into space before abruptly returning to normal
- Unaware of surroundings and won’t respond
- Can be provoked by hyperventulation or stress
- 1st line = sodium valporate or ethosuximide
What are atonic seizures?
- ‘Drop attacks’ : brief lapses in muscle tone
- 1st : sodium valporate
- 2nd : lamotrigine
What are myoclonic seizures?
- Sudden brief muscle contractions usually when tired
- 1st : sodium valporate or in females = levetiracetam
What are infantile spasms ?
-Known as ‘west syndrome’
-Starts around 6mnths of age
-Characterised by clusters of full body spasms
-Tx : prednislone, vigabatrin
What is status epilepticus
-Seizure lasting >5 mins or >3 seizures in an hour
How is status epilepticus treated in hospital ?
-Secure airway
-High-conc oxygen
-Assess cardiac and resp function
-Check glucose levels
-Insert cannula
-IV lorazepam 4mg, repeat after 10 mins if seizures continues
-If seizure persists : IV phenobarbital or phenytoin
Give two medical options in community for status epilepticus
-Buccal midazolam
-Rectal diazepam
What parkinson medication is associated with pulmonary fibrosis ?
-Cabergoline
What is used in the management of drug-induced parkinsonism
-Procyclidine
What artery is affected in amaurosis fugax?
-Central retinal/opthalmic artery
-Will be caused by atherosclerosis of the internal carotid on the SAME side as the amourosis
What antiparkinsonian medications are associated with disinhibition disorders ?
-Dopamine receptor agonists (e.g. bromocriptine/rotigotine/cabergoline))
What is Bell’s palsy
-Unilateral lower motor neurone facial nerve palsy
-Nerve is affected on the same side as the symptoms (e.g. dropping smile to the left, cannot close left eye or wrinke left side of forehead) = left cranial nerve VII LMN lesion
How is Bell’s palsy managed ?
-If pt presents within 72 hrs of sx onset = prednislone
-50mg for 10 days, then 60mg for 5 days, followed by reducing regime of 10mg a day
-Eye treatment : lubricating eye drops to prevent exposure keratopathy
You are examining a patient who complains of double vision. Whilst looking forward the patient’s left eye turns towards the nose. On looking to the patient’s right there is no obvious squint. However, on looking to the left the patient is unable to abduct the left eye and double vision worsens. What is the most likely underlying problem?
Left 6th nerve palsy
Define wernicke’s dysphasia
-Speech fluent, comprehension abnormal, repetition impaired
-It is from damage to the wenicke’s area in the temporal lobe
What tumours most commonly spread to the brain (5)
-Lung (most common)
-Breast
-Kidney
-Melanoma
-Colorectal cancer
What are the RF for idiopathic intracranial hypertension ?
-Obesity
-Female sex
-Pregnancy
-Drugs : COCP, steroids, tetracyclines, lithium, vit A
-Exam : young, overweight female
How does idiopathic intracranial hypertension present ? (5)
-Headache
-Blurred vision (reduced visual acuity)
-Papilloedema
-Enlarged blind spot
-VI nerve palsy may be present - LR6 - unable to abduct eye
How is idiopathic intracranial hypertension managed ?
-Weight loss
-Diuretics (e.g. acetazolamide)
What is the classic history in an acoustic neuroma (vestibular schwannoma)
-Vertigo, hearing loss, tinnitus and absent corneal reflex
-Corneal reflex : involuntary blinking caused by stimulation of cornea
-Account for 90% of cerebellopontine angle tumours (MRI is Ix of choice)
What is the most likely visual impairment seen in a pt with acromegaly ?
-Bi temporal hemianopia
-Pituitary lesion is often the cause = compression of optic chiasm
What questionnaire is used to diagnose neuropathic pain ?
-DN4
>4 = neuropathic pain
What 4 medications are used 1st line in neuropathic pain
-Amitriptyline
-Duloxetine
-Gabapentin
-Pregbalin
Give 7 features of complex regional pain syndrome
Neuropathic pain
Skin flushing
Swelling
Abnormal hair growth
Colour change
Temp change
Explain the pathway of the facial nerve
-Brainstem -> cerebellopontine angle - temporal bone and parotid gland
What are the 5 branches of the facial nerve
-Temporal
-Zygomatic
-Buccal
-Marginal mandibular
-Cervical
What is the motor function of the facial nerve
-Muscle of facial expression, the strapedius, posterior digastric, styohyoid and platysma muscle
What is the sensory function of the facial nerve
taste from anterior 2/3 of the tongue
What is the parasympathetic function of the facial nerve
-Supply to submandibular and sublingual salivary glands
-Lacrimal gland
What causes a unilateral upper motor facial nerve lesion
-STROKE
-tumour
How would an upper motor neurone facial lesion present and why
-Forehead sparing -> each side of the forehead receives upper motor innervation from both sides of the brain
What can cause lower motor neuron facial lesions
-Bell’s palsy
-Ramsay-hunt syndrome
What causes Ramsay-Hunt syndrome
Varicella Zoster Virus - causes inflammation and irritation of facial nerve
How does Ramsay-Hunt present
-unilateral lower motor neuron facial nerve palsy
-Painful, tender vesicular rash in the ear canal, pinna and around ear on affected side
-Rash to anterior 3/3rd of tongue and hard palate
- sensorineural deafness
- vertigo
How is ramsay-hunt treated
-Prednisolone
-Aciclovir
-Within 72 hrs
What is the inheritance pattern of Huntington’s
-Autosomal dominant
What causes Huntington’s
-Trinucleotide repeat disorder -> genetic mutation in the HTT gene on chromosome 4 (CAG)
what is anticipation
Successive generations have more repeats in the gene resulting in earlier age of onset and increased severity of disease
- Cognitive, psychotic or mood problems
- Chorea
- Eye movement disorders
- Speech difficulties (dysarthria)
- Swallowing difficulties (dysphagia)
=Huntington’s
EEG in absence seizures
Treatment
-> Bilateral, symetrical 3Hz spike and wave pattern
-> Sodium valporate and ethosuximide
What kind of aphasia is wernicke’s aphasia
receptive
Sentences that make no sense, word substitutions and neologisms but speech is fluent
Comprehension is impaired
Wernicke’s aphasia
What causes wernicke’s aphasia
-Lesion of superior temporal gyrus
-Supplied by inferior division of left MCA
What kind of aphasia is broca’s aphasia
Expressive
speech is non fluent, laboured and halting
Repetition is impaired
Comprehension is normal
Broca’s aphasia
What causes broca’s aphasia
-Lesion in inferior frontal gyrus
-Supplied by superior division of MCA
Conduction aphasia
-> Speech is fluent but repetition is poor. Comprehension is normal
-> Cause by stroke affecting arcuate fasiculus
What is global aphasia
-Large lesion affecting broca’s, wernicke’s and arcuate fasiculus
-> Faecal impaction, bladder distention leading to extreme HTN, flushing, sweating, agitation.
-Autonomic dysregulation due to spinal cord lesion at, or above T6.
- It is an uninhibited sympathetic nervous system response to a variety of noxious stimuli
What are the nerve roots of the brachial plexus and what are it’s sections
-C5 to T1
-Roots, trunks, divisions, cords, branches
REAL TEENAGERS DRINKS COLD BEERS
Damage to C5,6 roots
Winged scapula
Breech presentation possible cause
Erb-Duchenne paralysis
Damage to T1
Loss of intrinsic hand muscles
Due to traction
Klumpke’s paralysis
Sensory inattention
Apraxias
Astereognosis : inability to recgonise objects by touch
Inferior homonymous quadrantanopia
Parietal lobe lesion
Homonymous hemianopia (with macula sparing)
Cortical blindness
Visual agnosia
Occipital lobe lesions
Wernicke’s aphasia
Superior homonymous quadrantopia
Auditory agnosia
Prosopagnosia
Temporal lobe lesion
Broca’s aphasia
Disinhibition
Perseveration
Anosmia
Inability to generate list
Frontal lobe lesion
What tumour is associated with neurofibromatosis type 2
Bilateral vestibular schwannomas
What is the most common primary brain tumour
Glioblastoma
Solid tumours with central necrosis
What kind of brain tumour will cause symptoms of compresion rather than invasion
-Meningioma
What does brown-sequard syndrome cause
-Ipsilateral UMN weakness below lesion (corticospinal)
-Ipsilateral loss of proprioception and vibration sensation (dorsal)
-Contralateral loss of pain and temp sensation (spinothalamic)
=Lateral hemisection of the spinal cord
Define cataplexy
Sudden and transient loss of muscular tone caused by strong emotion
Ranges from buckling knees to collapse
What 3 things travel through the cavernous sinus
-Abducens nerve
-carotid plexus
-Internal carotid artery
What 3 things travel through the lateral wall of the cavernous sinus
Oculomotor nerve
Trochlear nerve
Opthalmic and maxillary branch of trigeminal nerve
do cerebellar lesions cause ipsilateral or contralateral signs
Ipsilateral
Give 6 signs of cerebella syndrome
D : dysdiadochokinesia
A : ataxia
N : nystagmus
I : intention tremor
S : slurred speech, scanning dysarthria
H : hypotonia
Where is CSF produced
Ependymal cells in choroid plexus
explain the circulation of the CSF
- Lateral ventricles (via foramen of munro)
- 3rd ventricle
- Cerebral aqueduct
- 4th ventricle (via foramina of magendie and luschka)
- Subarachnoid space
- Reabsorbed into venous system via arachnoid granulations into superior sagittal sinus
What nerve causes foot drop
-> Common peroneal nerve lesion (branch of sciatic nerve)
-> Injury often occurs at neck of fibula
-> Inability to dorsifelx foot
-> Sensory loss over the dorsum of the foot
Rapid onset dementia
Myoclonus - quick, involuntary muscle jerks
65yrs old
- Creutzfeldt-Jakob disease
- Caused by prion proteins that induce formation of amyloid folds resulting in tightly packed beta-pleated sheets
pain in the neck, upper or lower limbs
Loss of digital dexterity
Numbness
Urinary or faecal incontinence
Degenerative cervical myelopathy -> osteoarthritic changes causing narrowing of the cervical spine = compression
What is a test for degenerative cervical myelopathy and what is the gold standard investigation
-Hoffman’s sign : flicking one finger results in reflex twitching of other fingers on same hand
-Cervical spine MRI : disc degeneration and ligament hypertrophy
How is degenerative cervical myelopathy treated
Decompressive surgery
What is the nerve roots of the nipple? (dermatome)
T4 at the Teat Pore
What is the nerve root of the umbilicus
T10
BellybuT-TEN
What is the nerve root of the knee caps
L4
Down on aLL fours
What is the nerve root of the big toe and dorsum of foot
L5
Largest of the 5 toes
What is the nerve root of the little toe and lateal foot
S1
Smallest toe
Nerve root of thumb and index ringer
C6
Make a 6 with left hand by touching thumb to index finger
Nerve root of middle finger and palm
C7
Nerve root of ring and little finger
C8
Nerve root of inguinal ligament
L1
L for Ligament
1 for 1nguinal
Name 5 drugs that cause peripheral neuropathy
AMY : amiodarone
MET : metronidazole
NATHAN : nitrofurantoin
VIA : Vincristine
INSTAGRAM : Isonizid
Epilepsy and DVLA
- Inform DVLA
- First seizure : 6 mnths off
- Established epilepsy : apply for licence if 12 mnth seizure free
Stroke and DVLA
-1 mnth off driving
-No need to inform DVLA
Progressive muscular weakness from 5 yrs
Calf pseudohypertrophy
Gower’s sign : child uses arms to stand from squatted position
Intellecutal impairment
X linked recessive
Duchenne msucular dystrophy
-Fever, headache, psychiatric symptoms, iritability
-seizures, vomiting
Focal features (e.g. aphasia)
Encephalitis - if EBV : aciclovir
words enter in your ear and goes to wernickes in the temporal lobe to comprehend what was said, before travelling to broca’s area in the frontal lobe to generate speech
good way to remember
Most common cause of encephalitis in adults
-HSV-1 : typically affects temporal lobes
What is seen on CSF in encephalitis
Lymphocytosis
Elevated protein
How is encephalitis treated
IV aciclovir
Affected eye deviates up and out
Vertical diplopia (reading a book/going upstairs)
Head tilt
Fourth nerve palsy
SO4 -> superior oblique (superior oblique usually depresses eye and moves in)
10-15 yrs old
Gait ataxia
Kyphoscoliosis
Friedreich’s ataxia
What are the 3 modalities of the GCS
Motor response
Verbal response
Eye opening
Explain the possible motor response for the GCS
- Obeys commands
- Localises to pain
- Withdraws from pain
- Abnormal flexion to pain
- Extending to pain
- None
Explain the verbal response in the GCS
- Orientated
- Confused
- Words
- Sounds
- None
Explain the eye opening options in the GCS
- Spontaneous
- To speech
- To pain
- None
What causes lateral medullary syndrome (wallenberg’s)
-Occlusion of the posterior inferior cerebellar artery
What cause neuroleptic malignant syndrome
-Occurs in patients taking antipsychotic medications
How does neuroleptic malignant syndrome present `
Within hrs/days of starting an antipsychotic
Pyrexia/hyperthermia
Muscle rigidity
Autonomic instability : hypotension & tachycardia
Agitate delirium with confusion
What might be seen on the bloods in neuroleptic malignant syndrome
-Raised creatinine kinase + raised urea = AKI
-Leukocytosis
-AKI secondary due to rhabdomyolysis
Urinary incontinence
Dementia and bradyphrenia
Gait abnormality similar to parkinson’s (e.g. shuffling or broad-based)
Normal pressure hydrocephalus
Treated with a shunt or acetazolamide (carbonic anhydrase inhibitor)
Give 4 metabolic abnormalities that occur in refeeding syndrome
Hypophosphataemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance
Give 3 causes of a peripheral neuropathy causing predominantly motor loss
-GBS
-Lead poisoning
-Charcot marie tooth
Give 4 causes of a peripheral neuropathy causing predominantly sensory loss
A : alcohol
B : B12 deficiency
C : cancer and CKD
D : DM and drugs *
E : every vasculitis
Give 4 features that favour pseudoseizures over true seizures
Pelvic thrusting
Crying after seizures
Don’t occur when alone
gradual onset
Give 2 features that factors true seizures
Tongue biting
Raised serum prolactin
Give 5 causes of raised ICP
Idiopathic
Traumatic
Infection - meningitis
Tumour
Hydrocephalus
How is raised ICP managed
-Simple management : elevate head of bed to 30 degrees
-IV mannitol : osmotic diuretic
Controlled hyperventilation
Removal of CSF
Give the reflexes and the nerve root
Ankle : S1-S2
Knee : L3-L4
Biceps : C5-C6
Triceps : C7-C8
2 year old
Preceding viral illness
Encephalopathy : confusion, seizures, oedema, coma
Fatty infiltration of the liver, kidneys and pancreas
Hypoglycaemia
Reye’s syndrome
Eye deviated down and out
Ptosis
Third nerve palsy
Explain the homonymous quadrantanopias
PITS
-> Parietal lobe - inferior
-> Temporal lobe - superior
Cause of bitemporal hemianopia
-Lesion of optic chiasm, often pituitary tumour
Cause of homonymous hemianopia causing incongruous defects
Lesion of optic tract
Left homonymous hemianopia = lesion of right optic tract
Cause of homonymous hemianopia with incongruous defects
-Lesion of optic radiation or occipital cortex
-Macula sparing : occipital cortex
- Left sided CN III palsy - ptosis and fixed dilation pupil pointing down and out
- Right sided arm, hip and knee weakness
- Right sided hyperreflexia
-Weber’s syndrome - midbrain stroke - ipsilateral CN III palsy and contralateral hemiparesis
-Left posterior cerebral artery
Contralateral homonymous hemianopia
Macular sparing
Visual agnosia
Posterior cerebral artery
Teenager
Hypersomnolence
Sleep paralysis
Vivid hallucinations on going to sleep or waking up
Narcolepsy
Ix : multiple sleep latency EEG
Tx : daytime stimulant (e.g. modafinil) and nighttime sodium oxybate
Bell’s palsy hasn’t resolved in 3 mnths, what should be done?
Refer urgently to ENT or a neurologist
sensation loss : fine touch, proprioception, vibration
Dorsal column
What is used to measure disability or dependence in activities of daily living in stroke patients
Barthel index
Which of the following features is typically spared in this condition :
Breathing difficulties
Emotional lability
Opthalmoplegia
Slurred speech
Swallowing difficulty
Opthalmoplegia
Peropheral ‘finger-nose ataxia’
Cerebellar hemisphere lesion
Gait ataxia
Cerebellar vermis lesion
Lamotrigine : mechanism of action, adverse effects
sodium channel blocker
stevens-johnsons syndrome
- onset ~ 65
- Postural inastability and falls
- atypical parkinson syndrome : tau
- Cognitive impairment
- Impairment of vertical gaze
progressive supranuclear palsy
Give 3 ascending tracts of the CNS
DCML
Spinothalamic
Spinocerebllar
What in formation does the DCML transport
vibration, proprioception and fine touch from from the body to the brain
what information does the anterior spinothalamic tract carry
crude touch and pressure
what information does the lateral spinothalamic tract carry
pain and temperature
what information does the spinocerebellar tract carry
proprioceptive signals : info about muscle stretch and the rate of muscle stretch
what information do descending tracts carry in the CNS
Motor info
what are upper motor neurones
Carry motor info from the brain and brainstem to the ventral horn of the spinal cord
what are lower motor neurones
They carry motor info from the spinal cord to peripheral muscles
what are pyramidal tracts
Descending tracts
They pass through the pyramids of the medulla oblongata
Voluntary, conscious control of body and face muscles
Corticospinal : cortex to body
Corticobulbar : cortex to bulb
Explain the pathway of the corticospinal tract
-Info from pimary motor cortex, premotor cortex coverage to for internal capsule
-The CST then passess through the pons and caudal medulla where it divides
-Lateral CST : decussates in pyramid of medulla
-Anterior CST : stays ipsilateral
-Tracts descend into the spinal cord, terminating at ventral horn where they synapse with LMN to peripheral muscle
what are extrapyramidal tracts
Originate in brainstem, don’t pass through pyramids
Unconscious, reflexive movement of muscle to control balance, locomotion, posture and tone
4 types : reticulospinal, vestibulospinal, rubrospinal and tectospinal
impaired adduction of the eye on the side of the lesion
horizontal nystagmus of abducting eye on contralateral side
internuclear opthalmoplegia : caused by MS or vascular disease
and is due to lesion in medial longitudinal fasciculus (MLF)
give a common presentation of tuberous sclerosis
child presenting with epilepsy found to have skin features of tuberous sclerosis
which limbs are more affected in an anterior cerebral artery stroke
Lower limbs
Which limbs are more affected in a middle cerebral artery stroke
Upper + associated aphasia
what is the best imaging for a TIA
Diffusion-weighted MRI
Wrist drop is associated with damage to what nerve and what kind of injury
- Radial nerve
- Fracture of the shaft of the humerus
- Or compression of nerve against humerus after sleeping on arm.
Damage to what cranial nerve will cause an absent of corneal reflex : no blinking or tearing on application of cotton wool
CNI
-Headache worse when upright, better on lying down
-PMH : marfan’s
-Spontaneous intracranial hypotension
-Headahce cause by CSF leak -> MRI with gadolinium shows pachymeningeal enhancement
what GCS would suggest need for intubation
<8
what is given 1st line for spasticity in MS
Baclofen and gabapentin
what is a common cause of bilateral foot drop
-Peripheral neuropathy
-Presents with ‘high-stepping’ gait
During trauma, fluid draining from the nose or ear is tested for what to determine if it is CSF
Glucose
Beta-2-transferrin is gold standard
what type of medications are levodopa and other antiparkinsons medications ?
‘critical’ medications
They must always be given on time and not stopped on acute admission
give 3 drugs that ca cause SJS
CARBAMAZEPINE
Lamotrigine
Allopurinol
-Painful third nerve palsy -> down and out eye with painful eye movement
-Headache and blurred vision
-Dilated pupil unresponsive to light
Posterior communicating artery aneurysm
what is becker muscular dystrophy
Less severe form of muscular dystrophy
develops after the age of 10
pseudohypertrophy and + GOWER’S SIGN
give 6 drugs that can cause idiopathic intracranial hypertensions
COMAAR
C : ciclosporin
O : oral contraceptives
M : mineralocorticoids
A : amiodarone
A : antibiotics
R : retinoic acid
what is seen on neuroimaging in normal pressure hydrocephalus
Ventriculomegaly with relative preservation of cortical sulci
Initial signs of degenerative cervical myelopathy
Neck pain
Stiffness
Reduced range of motion
Progressive signs of degnerative cervical myelopathy
-Shooting pains from neck, down the spine
-Weakness in arms and hands
-Numbness and tingling in arms and hands
-Clumsiness and poor coordination
-Difficulty handling small objects (pens, coins, phone)
-Balance issues
common exam question for degnerative cervical myelopathy
lower limb stiffness and imbalance
previous misdiagnosis of carpal tunnel (unresponsive to treatment)
define myelopathy
-Injury to the spinal cord due to severe compression
-Can be due to trauma, congenital stenosis, degenerative disease or disc herniation.
How would a posterior inferior cerebellar artery stroke (wallenberg/lateralk medullary syndrome) present
-Ipsilateral : facial pain and temp loss
-Contralateral : limb/torso pain and temp loss
-ATAXIA, NYSTAGMUS
How would an anterior inferior cerebella artery stroke present (lateral pontine syndrome)
Ipsilateral facial paralysis and deafness
Other symptoms similar to wallenbergs
how does HSE present and what is seen on CT
-Prodrome : fever, headahce and malaise
-Acute encephalopathy : focal neurological deficits, seizures, confusion and behavioural changes
-Bilateral temporal lobe changes
Subacute
Bilateral
Fine touch
vibration
Syirngomyelia
motor
loss of pain and temp
- Severe unilateral headache
- Scalp tenderness
- Jaw claudication
- Amaurosis fugax
Temporal / giant cell arteritis
what is strongly associated with GCA
- Polymyalgia rheumatica
how is GCA diagnosed
- Raised ESR
- Multinucleated giant cells on temporal artery biopsy
How is GCA managed
- 60mg pred is visual / jaw sx
- 40mg pred if not
TIA : most common cause, imaging, management
- AF
- Diffusion-weight MRI
- 300mg aspirin
- Can’t drive for 4 weeks
what secondary prevention is used in a TIA
- 75mg clopidogrel
- 80mg statin
- Carotid endarecetomy if >70% stenosis
First line tx for alzheimer’s
- Donepezil (AChE inhibitor)
- Memantine if severe (NMDA antagonists)
what antidepressants can worsen cognition in alzheimer’s
TCA’s
Cauda Equina : cause
- Causes : trauma, infection, herniation of lumbar disc
Cauda Equina : presentation (5)
- Bilateral sciatica
- Bowel/bladder dysfunction
- Saddle parastesia
- Lower limb weakness/sensory deficit
- Sexual dysfunction
What is thoracic outlet syndrome and how might it present
- Compression of brachial plexus, subclavian artery or subclavian vein at site of thoracic outlet
- Young woman with dropping shoulders and long neck
3 possible presentations and thoracic outlet syndrome
- Brachial plexus : pain;ess muscle wasting of the hand, numbness and tingling
- Subclavian artery : painful claudication of arm leading to ulceration and gangrene
- Subclavian vein : painful diffuse arm swelling and distended veins
Injury following fall onto outstretch wrist
- Median nerve injury : inability to extend wrist or abduct thumb
- Ex : female, hx of MH disorder
- Px : pelvic thrusting, gradual onset, emotional and upset after seizure
- Ix : no abnormal EEG activity
functional seizure / NEAD
Unilateral vision loss, pain, red eye, N&V
Glaucoma
constantly adducted eye
CN VI palsy
Ptosis, Miosis, Anhidrosis
Horner’s syndrome : damage to sympathetic nervous system
give 4 central lesion causes of horner’s
4 S’s : anhidrosis of arm, trunk and face
- Stroke
- MS
- Swelling (tumours)
- Syringomyelia
give 4 pre-ganglionic causes of horner’s
4 T - arise from spinal cord in chest, causes anhidrosis of face
- T : Tumour (Pancoast)
- T : Trauma
- T : Thyroidectomy
- T : Top rib
Give 4 post ganglionic causes of horner’s
4 C’s : travel to the head alongside internal carotid, do not cause anhidrosis
- C : Carotid aneurysm
- C : Carotid artery dissection
- C : cavernous sinus thrombosis
- C : cluster headache
test for horners
- Cocaine eye drop : no change in pupil
- Px : ‘please look to the left’ : one eye completely fails to adduct, the other shows nystagmus while abducting
Internuclear opthalmoplegia
what causes internuclear opthalmoplegia and what can it be a common sign of
- Lesion of medial longitudinal fasciculus
- MS
give 6 RF for retinal detachment
- Male
- > 40
- Prev ocular surgery
- Fx
- Retinal detachment in other eye
How does retinal detachment present
- Painless vision loss
- Flashing lights
- Floaters
- ‘Cobwebs in periphery’
- Curtain over part of eye
how is retinal detachment Ix and Tx
- Ix : RAPD, altered red reflex, reduced acuity, visual field defects
- Tx : surgical repair
how does a central retinal artery occlusion present
- sudden painless loss of vision (seconds), cherry red spot in macula, pale optic disc, RAPD
what causes a retinal artery occlusion. amndhow is it treated
- clot from internal carotid into opthalmic artery
- Tx : ocular massage, IV mannitol, urokinase injection
what is cushing’s triad
- widening pulse pressure, braducardia, irregular breathing
- sign of raised ICP
If large enough what will pituitary tumours cause
bilateral hemianopia by pressing on optic chiasm
what tumours commonly metastasise to the brain
- lung
- breast
- renal cell carcinoma
- melanoma
charcots neurological triad
Triad of sx associated with MS
- Dysarthria
- Nystagmus
- Intention tremor
what regular medications are used in MS
- Dimethyl fumarate (mild)
- Alemtuzumab + natalizumab
- Immunosupression (betaferon)
how does sodium valporate work, 3 key SE
- Increases GABA activity
- Weight gain
- P450 enzyme inhibitor
- Teratogenic
how does carbamazepine work, 3 key SE
- Binds to sodium channels, increase refractory period
- P450 enzyme inhibitor
- Inappropriate ADH secretion
- Visual disturbance (diplopia)
How does lamotrigine work, key SE
- sodium channel blocker
- SJS
How can you elicit the myasthenic snarl
Count to 50 , then smile
what can be used to help spasms in MS
- Baclofen
