Neurology Flashcards
Difference between simple partial and complex partial seizure
Simple: awareness unimpaired
Complex: awareness impaired and post ictal confusion
Tonic clonic vs myoclonic seizures
Tonic clonic: limbs stiffen and jerk
Myoclonic: limbs just jerk
Causes of seziures
2/3rd idiopathic Space occupying lesion/stroke Trauma/haemorrhage/increased ICP Fever Infection Drugs
Things to ask in seizure history
Length of time/tongue biting/incontinence Prodrome Post ictal changes Triggers Previous seizures or first one? Family history Drug use
Differential diagnosis for transient loss of consciousness
Vasovagal syncope
Orthostatic
Cardiac abnormality/arrhythmia
Hypoglycaemia
Investigations for seizures
FBC, glucose, Ca, electrolytes, Creatinine, LFTs Urine toxocology screen CXR Consider LP CT head EEG/MRI in certain patients
Non pharmacological management of seizures
Avoid triggers Avoid driving for 1 year seizure free Avoid swimming, heights, heavy machinery Refer to first seizure clinic Epilepsy nurse specialist
Pharmacological management of seizures
Usually commenced by neurologist after 2nd seziure
Generalised: sodium valproate, lamotrigine
Partial: carbamazepine, levertiracetam
Pregnant or breastfeeding: Lamotrigine
Neurosurgical resection if clear epileptogenic focus
Distinguishing features of motor neurone disease
No sensory loss
Upper and lower motor neurons affected
Eye movements never affected
Name the 4 types of motor neurone disease
Amyotrophic lateral sclerosis: most common, upper and lower motor neuron signs, bladder spared
Progressive bulbar palsy: only affects cranial nerves 9-12
can be bulbar or corticobulbar
Progressive muscular atrophy: only LMN signs
Primary lateral sclerosis: Predominately UMN signs and no cognitive decline
Differentials for motor neuron disease
Peripheral neuropathy Myopathies Post polio syndrome Myasthenia gravis Brain or spinal cord lesion
Investigations for motor neuron disease
MRI
Nerve conduction studies
Management of MND
Poor prognosis-multi disciplinary approach Antiglutamatergic drugs (riluzole) Amitriptylline for drooling Consider NG/PEG Baclofen/diazepam for spasticity
Pathogenesis of MS
Plaques of demylination caused by a T cell mediated immune response
Primarily clinical diagnosis but can use MRI and oligonal bands on LP
Presentation of MS
Solo Neurological deficit which comes then goes, eg. weakness in a leg, optic neuritis, ataxia, parasthesia
Family history of MS
What are you looking for on examination for MS
Spastic paraparesis Sensory loss Nystagmus Impaired co-ordination Ataxic gait Failure of rhomburg test Ophthalmoplegia Decreased visual acuity Lhermitte's sign
Investigations for MS
MRI
Evoked response testing of nerves
CSF (oligoclonal IgG bands on electrophoresis)
Management of MS
Symptomatic management
Interferons decrease relapse frequency
Steroids in acute relapses
Methotrexate and aziothioprine can be trialled
Pathogenesis of Myasthenia gravis
Autoimmune disease against acetylcholine receptors on post synaptic membranes which inhibits muscle contraction
Presentation to ask about with myasthenia gravis
Drooping eyelids
Difficulty chewing/swallowing
Proximal muscle weakness
Ask about other autoimmune diseases
Things to check on examination for myasthenia gravis
Ptosis peek sign Sustained upward gaze Thymectomy scar Weakness of neck flexion
Investigations for myasthenia gravis
Acetylcholine esterase antibodies
Electromyogram
Thymoma investigation (cxr or thoracic CT)
Respiratory function tests
Management of myasthenia gravis
Pyrodostigmine (causes increased drooling and crying)
Sudden worsening respiratory symptoms can be life threatening
Relapses treated with prednisone-often needed long term so give osteoporosis prophylaxis
If steroids fail give immunosuppresion with methotrexate or azathioprine
Thymectomy
Key signs of parkinson’s
Tremor
Rigidity
Akinesia/bradykinesia
Postural instability
Pathogenesis of parkinson’s
Depletion of dopaminergic cells in pars compacta in substantia nigra
Name some prodromal premotor symptoms of parkinson’s
Anosmia Depression Insomnia Autonomic effects Dribbling
Extra tests for parkinson’s on examination
Glabellar tap Occular movements Lying and standing BP Undo buttons write name
What are the parkinson’s plus syndromes
Progressive supranuclear palsy: early postural instability and vertical gaze palsy
Multisystem atrophy: Cerebellar signs
Lewy body dementia: hallucinations
Cortico-basal degeneration: akinetic rigidity affecting one limb
Which drugs can induce parkinsonism
Haloperidol and lithium
Wilson’s disease
Investigations for parkinsonism
MRI to exclude brain lesion
Levodopa challenge
Management of parkinsonism
Multidiscip
Levodopa (can cause pychosis)
Dopamine agonists (ropinerole)
Anticholinergics help with tremor (but cause confusion, dry mouth and urinary retention)
Deep brain stimulation
Surgical ablation of overactive basal ganglia
What causes a TIA?
Atherothromboembolism
Cardioembolism
Hyperviscosity
Investigations for TIA
FBC, ESR, U+E's, glucose, lipids CXR Carotid ultrasound CT ?Echo ECG
How do we calculate stroke risk score after TIA?
ABCD2 Age >60 Blood pressure >140/90 Clinical features (unilateral weakness/speech disturbance) Duration of symptoms >1 hour Diabetes
Management of TIA
Avoid driving for a month
Diet and exercise
Control CV risk factors
Aspirin 300mg daily and clopidogrel 75mg daily
Consider carotid endarterectomy if >70% stenosed
How do the causes differ for the two types of stroke?
Ischaemic: artherosclerosis and thromboemboli
Haemorrhagic: hypertension, berry aneurysm, av malformation
Exam findings in a stroke caused by internal carotid artery
Hemiparesis on opposite side of the body and homonymous hemianopia
Dysphasia
Exam findings in a stroke caused by anterior cerebral artery
Hemiparesis in legs
sensory loss in legs
change in personality/mood/behaviour
Exam findings in a stroke caused by middle cerebral artery
Weakness on opposite side of the lower face and arms, can have aphasia
Exam findings in a stroke caused by posterior cerebral artery
Homonymous hemianopia
problems with spatial skills and recognition
problems with memory and mood
Exam findings in a stroke caused by midbrain
cranial nerve 3 and 4 deficits on SAME SIDE plus weakness and sensory loss on opposite side
Exam findings in a stroke caused by medulla
cranial nerve 5 and 6 deficits on SAME SIDE plus weakness and sensory loss on opposite side
Exam findings in a stroke caused by cerebellum
DASHING Dysdiadochokinesia Ataxia Slurred speech Hypotonia Intention tremor Nystagmus Gait abnormality
Investigations for stroke
FBC, electrolytes, creatinine, glucose, lipids, coag screen Blood cultures if febrile ECG ?AF CT Carotid USS Echo if young and ?cause
Management of acute ischemic stroke on discharge
Protect airway- exclude haemorrhagic stroke Give IV alteplase if within 4.5 hours Clopidogrel 75mg Consider heparin DVT prophylaxis Driving restriction Statins Consider carotid endartectomy
Management of acute haemorrhagic stroke
Stop antithrombotics
Reverse anticoagulation
Neurosurgical referral
What are some key causes of polyneuropathy
Diabetes Renal failure Low B12 and B1 Isoniazid/phenytoin Guillan barre syndrome HIV/Syphilis
key things to ask in polyneuropathy history
Time course Preceding events Travel Drugs Sexual infections Family history
How to differentiate between sensory, motor and autonomic neuropathy
Sensory: numbness, burning, tingling, glove and stocking
Motor: progressive, weakness, wasting, reduced reflexes
Autonomic: ED, decreased sweating, urinary retention, homes adie pupil (dilated and unresponsive to light)
Investigations for polyneuropathy
FBC, ESR, glucose, TSH, b12/folate, ANA, ANCA CXR Consider LP Urinalysis Nerve conduction studies
management of polyneuropathy
Treat underlying cause
foot care
Amitryptilline/gabapentin for neuropathic pain
Guillan barre syndrome pathogenesis
Acute inflammatory demyelinating polyneuropathy, often caused by campylobacter or EBV
Symptoms progress for 4 weeks then resolve
Presentation of Guillan barre symptoms
Progressive muscle weakness over days Areflexia Pain Speech Facial droop Autonomic dysfunction
Investigations for guillan barre
Nerve conduction studies LP Bloods (check campylobacter serology) Spirometry MRI spinal cord
Diagnostic criteria for guillan barre
Progressive muscle weakness in limbs
Areflexia
Progressive sensory change over 2-4 weeks
Treatment for guillan barre
IV IG Plasma exchange Ventilate if severe respiratory involvement DVT prophylaxis Monitor vitals Follow every 4-6 weeks for 6 months
Prognosis/complications for guillan barre
85% good recovery but 20% mortality if ventilated
Can have respiratory failure, Ileus and bladder issues
What are the three most common muscular dystrophies?
Duchenne’s muscular dystrophy
Fascioscapulo humeral muscular dystophy
Becker’s muscular dystrophy
What is the most common myotonic disorder?
Dystrophia myotonica Distal onset weakness facial weakness/wasting Diabetes Male frontal baldness Most patients die in middle age
Work up of code stroke
?symptoms worst at onset ?sudden onset How long since last seen well ?anticoagulants ?malignancy ?pregnancy ?prior stroke ?haemorrhage Take BP and determine NIHSS CT head CT angiography CT perfusion
