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