Neurology Flashcards
Glascow coma score
Eyes 4 - spontaneous opening 3 - opens on command 2 - opens in response to pain 1 - no opening
Verbal 5 - normal speech 4 - confused 3 - incoherent speech 2 - incomprehensible sounds 1 - no sounds
Motor 6 - norma movement 5 - localisation towards pain 4 - withdrawal from pain 3 - flexor response to pain 2 - extensor reponse to pain 1 - no movement
LMN lesion
Tone - flaccid Involuntary movement - fasciculations Reflexes - decreased Platar reflex - downgoing Weakness - present
UMN lesion
Tone - spastic Involuntary movement - none Reflexes - increased Platar reflex - up-going Weakness - present
Extrapyramidal lesion
Tone - rigid Involuntary movement - tremor Reflexes - normal Platar reflex - down going Weakness - absent
Muscle strength grading
5 - full power 4 - submaximal power against resistance 3 - full ROM against gravity withou resistance 2 - full ROM without gravity 1 - muscle flicker 0 - no muscle contraction
Neuromuscular disease overview
Motor neuron disease Weakness - segmental and asymetrical, distal->proximal Fasciculations - yes Reflexes - increased Sensory - no Autonomic - no EMG - denervation and reinervation NCS - normal Muscle enzyme - normal
Peripheral neuropathy Weakness - distal (except GBS) but may be assymetrical Fasciculations - yes Reflexes - decreased/absent Sensory - yes Autonomic - yes EMG - signsof demyelination+ axonal loss NCS - abnormal Muscle enzyme - normal
Neuromuscular junction Weakness - proximal and fatiguable Fasciculations - no Reflexes - normal Sensory - no Autonomic -no EMG - decremental response in MG, jitter on single fibre EMG NCS - normal Muscle enzyme - normal
Myopathy Weakness - proximal Fasciculations - no Reflexes - normal Sensory - no Autonomic -no EMG - small, short motor potentials NCS - normal Muscle enzyme - increased
Lumbar puncture
Samples Tube #1 cell count and differential Tube #2 chemistry: glucose and protein Tube #3 microbiology: gram stain + culture Tube #4 cytology Tube #5 cel count: compare to tube #1
Normal
- clear
- protein <0.45g/L
- glucose 60% of serum glucose, >3.0mmol/L
- 0-5 WBC, 0RBC, 0 neutrophil
Viral infections
- normal or slightly increased proteins <1g
- normal glucose
- <1000x10^6/L cells, lymphocytes mostly
Bacterial infections
- opalescent yellow
- increased protein >1g
- decreased glucose
- > 1000x10^6/L cells, mainly PMN
Granuomatous infections
- clear or opalescent
- increased protein but <5g/L
- decreased glucose
- <1000x10^6/L cells, mainly lymphocytes
Olfactory nerve deficits
Absence of smell
DDx:
- nasal obstructions
- olfactory neuroepithelial: destruction by viral infections
- central: Kallman’s syndrome, head injury, cranial surgery
- endocrine/metabolic: DM, adrenal dysfunction, vitamin deficiency
Optic nerve deficits
Acute visual loss
DDx
- Opthalmologic: acute angle closure glaucoma, vitreous hemorrhage, retinal detachment, uveitis, trauma
- Infection/inflammation: endophthalmitis
- Optic nerve; optic neuritis, anterior ischemic neuropathy, compression
- Vascular: TIA/amaurosis fugax, central retinal artery or vein occlusion, carotid-cavernous sinus fistula
- CNS: stroke, optic tract/chiasm lesion, migraine
Oculomotor nerve deficits
Ptosis, resing position depressed and abducted, dilated pupil. Vertical and horizontal diplopia
DDx
- Midbrain: complete unilateral 3rd nerve palsy, weakness of superior rectus and ptosis, contralateral pyramidal/cerebellar signs
- Posterior communicating artery aneurysm: early dilation of pupil, then CNIII palsy
- Cavernous sinus: associated with CN II, IV, VI, V1 and V2 deficits. Internal carotid aneurysm, meningioma, sinus thrombosis.
- Ischemia of CNIII: pupil sparing CN III palsy. DM, temporal arteritis, HTN.
Trochlear nerve deficits
Binocular vertical and torsional diplopia, downward and inward gaze. Difficulty going down stairs or reading.
DDx
- Common: ischemic, idiopathic, trauma, congenital
- Others: cavernous sinus, superior orbital fissure
Trigeminal nerve deficits
Ipsilateral facial numbness, weakness of muscle of mastication with pterygoid deviation towards the lesion.
DDx
- Brainstem: ischemia, syringobulbia, demyelination
- Peripheral: tumour, aneurysm, metastatic infiltration
- Trigeminal ganglion: acoustic neuroma, meningioma, fracure o middle fossa
- Cavernous sinus
- Trauma
- Others: trigeminal neuralgia, herpes zoster
Abducens nerve deficits
Inward deviation, inability to abduct on affected side.
DDx:
- Pons: facial weakness and contralaeral pyramidal signs
- Tentorial orifice: alse localising sign of increased ICP
- Cavernous sinus
- Vascular
- Congenital: Duane’s syndrome
Facial nerve deficit
LMN lesion: ipsilaeral facial weakness demonstrated by facial droop, flatened forehead, inability to close eyes, flattened nasolabial fold.
UMN lesion: contralateral facial weakness with forehead sparing
impaired lacrimation, decreased salviation, numbness behind auricle, hyperacusis, taste dysfunction of anterior 2/3
DDx
- Idiopathic: Bell’s palsy
- Others: temporal bone fracture, EBV, Ramsey-Hunt, otitis media/mastoiditis, sarcoidosis, DM, paotid gland disease
Glossopharyngeal nerve deficit
Taste dysfunction in posterior 1/3 tongue. Absent gag reflex and dysphagia. Glossopharyngeal neuralgia, sharp pain of posterior pharynx radiaing to ear, triggered by swallowing.
Vagus nerve deficit
oropharyngeal dysphagia, dysarthria. Uvula and palateal deviation away from lesion.
Accessory nerve deficit
LMN lesion: paralysis of ipsilateral trapezius and sternocleidomastoid.
UMN lesion: paralysis o ipsilateral sternocleidomastoid and contralateral trapezius
Accessory nerve deficit
LMN lesion: paralysis of ipsilateral trapezius and sternocleidomastoid.
UMN lesion: paralysis o ipsilateral sternocleidomastoid and contralateral trapezius
Hypoglossal nerve deficit
LMN lesion: tongue deviation toward side of lesion, ipsilateral tongue atrophy, fasiculations
UMN lesion: absence of atrophy and fasiculations
Seizure
Terminology
- Provoked: fever, trauma, metabolic, neoplasm
- Unprovoked: no structrural or metabolic cause
Generalised seizures
- involves the entire brain, can be convulsive or non-convulsive (absence)
- Tonic-clonic: prodrome of unease or irritability hours before attack, tonic phase (muscle contraction, trunk hyperextension, cry from respiratory muscle spasm, last 30secs) followed clonic phase (violent jerking, tongue biting, frothing, incontinence), typically followed by several mins of deep unconsciousness and post-ictal confusion, headache.
- Absence: usually only in children, un-responsive or 5-10secs with arrest in activity, no post-ictal confusion
- Tonic: decreased LOC, muscle contraction, drop attacke
- Clonic: decreased LOC with repetitive jerks
- Myoclonic: brief contractions localised to muscle groups of one or more extremeties
- Atonic: loss of posture, dop attack
Partial seizure
- simple (no change in LOC) or complex (alteration of mood, memory, perception)
- Motor: jerking or sustained spasm of localised muscles
- Sensory: numbness, tingling
- Autonomic: epigastric discomfort, pallor, sweatin, piloerection
- Psychiatric: more commonly complex
Investigations
- FBC, glucose, U&E, LFTs, CRP, calcium, magnesium
Treatment
- Avoid precipitating facors
- Medical therapy if 2 or more unprovoked seizures in last 6 months, known organic brain disease, EEG wih epileptiform activity, first episode of status epilepticus
- General seizures: lamotrigine, valproate, topiramate
- Partial seizures: carbamazepine, gabapentin, phenytoin, tiagabine
- Absent seizures: ethosuximide
- Stop driving until seizure free for 12 months
Status epilepticus
Sustained seizure activity >30mins can result in brain damage.
Management
1. ABCs
2. Vital signs + blood glucose finger prick
3. Lab investigations: U&E, Ca, Mg, PO4, glucose, FBC, toxicology, anticonvulsant levels, lumbar puncture
4. 50% glucose 50mL + thiamine 100mg
5. Lorazepam 1mg/kg at 2mg/min
If not controlled:
- Phenytoin 20mg/kg IV at max rate of 50mg/min
- Phenobarbital 1000-1500 mg IV slowly
Delirium
Acute onset, disorientation, marked variability, fluctuating level of consciousness, poor attention, and marked psychomotor change.
Etiology
- Vascular: subarachnoid haemorrhage, stroke/TIA
- Infections: meningitis, encephalitis, abcess
- Traumatic: diffuse axonal shear, epidural hematoma, subdural hematoma
- Autoimmune: acute CNS vasculitis, SLE
- Neoplastic: mass effect/edema, hemorrhage, seizure
- Seizure: status epilepticus
- Primary psychiatric: psychotic disorder, mood disorder, anxiety disroder
Dementia
Acquired generalised and progressive impairment of cognitive function associated with impairment in usual activities of daily living. 15% of those >65 have dementia, 60-80% AD, 10-20% vascular dementia.
Etiology
- Alzheimer’s disease: memory imparment, asphasia, apraxia, agnosia
- Lewy body dementia: visual hallucinations, parkinsonism, fluctuating cognition
- Frontotemporal dementia: behavioural presentation (disinhibition, decreased social awareness, mental rigidity, memory spared), language presentation (progressive non-fluent aphasia, semantic dementia)
- Parkinsonism
- Huntington’s: chorea
- Multi-infarct dementia: stepwise or progressive deterioration
- CNS vasculitis: systemic signs of vasculitis
- Chronic meningitis
- Chronic encephalitis
- Chronic abscess
- HIV
- Creutsfelt-Jacob disease
- Syphilis
- Diffuse axonal shear, epidural hematoma, subdural hematoma
- SLE
- Neoplastic/paraneoplastic
Reversible causes:
- Alcohol intoxication, withdrawal, Wernicke’s encephalopathy
- Medication: benzodiazepines, anticholinergics
- Heavy metals
- Hepatic or renal failure
- Wilson’s disease
- B12 deficiency
- Hypo/hyperglycaemia
- Hypo/hypercortisol
- Thyroid dysfunction
- normal pressure hydrocephalus
- Depression
- Brain tumour
- Subdural hematoma
History
- geriatric giants: confusion, incontinence, falls, polypharmacy, memory, safety, pyschiatric
- ADLs and IADLs
- alcohol, smoking
- OTC, medications, compliance
- vascular diase and head trauma hx
- collateral Hx
Issues to consider
- failure to cope
- fitness to drive
- caregiver education and stress, respite services
- power of attorney
- wills
- advance directives
Alzheimer’s disease
Progressive cognitive decline interfering with social and occupational functioning characterised by :
1) anterograde amnesia - inability to learn new information
2) one of the following cognitive disturbance:
- asphasia: language disturbance
- apraxia: impaired ability to carry out motor activities
- agnosia: failure to recognise or identify new objects
- disturbance in executive functions
Pathophysiology
- genetic: minority <7% of AD cases are autosomal dominant inheritence
- pathology: diffuse cortical atrophy, senile plaques, neurofibrillary tangles
Risk factors:
- age
- family Hx of AD
- head injury
- low education level
- smoking
- Down’s syndrome
Features:
- cognitive impairment
- psychiatric manifestations: major depressive disorder, psychosis, apathy
- motor manifestation late in disease
Mean duration of disease 10yrs
Lewy body dementia
Progressive cognitive decline interfering with social or occupational function, memory loss not usually an early feature. 15-25% of all dementias. One or two of the following features:
- fluctuating cognition with pronounced variation in attention and alertness
- recurrent visual hallucinations
- parkinonism
Etiology
- Lewy bodies found in both cortical and subcortical structures
- mixed DLB and AD pathology common
Treatment
- acetylcholinesterase inhibitors
Typical survival 3-6yrs
Frontotemporal dementia
Third most common cause of cortical dementia. Behavioural variant is more common and presents with social conduct disorder. Language variant presents with disorder of expressive language.
Features:
Core features:
1) Insidious onset and gradual progression
2) Early decline in social interpersonal conduct
3) Early impairment in regulation of personal conduct
4) Early emotional blunting
5) Early loss of insight
Supportive features:
1) Behavioural
2) Speech and language
3) Physical signs
Imaging shows predominantly frontal and/or anterior temporal lobe atrophy
