Neurology Flashcards
What do the internal carotids supply?
Anterior 2/3rds of cerebral hemispheres and basal ganglia
What supplies the circle of willis?
internal carotids and basilar
What happens with a anterior cerebral artery occlusion?
frontal and medial cerebrum, weak contralateral legs (sometimes arms), facial sparing
What happens with a middle cerebral artery occlusion?
lateral part of each hemisphere, occlusion = contralateral hemiparesis, hemisensory loss, contralateral homonymous hemianopia, dysphasia, visuo-spatial disturbance
What happens with a posterior cerebral artery occlusion?
occipital lobe, contralateral homonymous hemianopia
What happens with a vertebrobasilar artery occlusion?
cerebellum, occipital brainstem; occlusion = hemianopia, cortical blindness, diplopia, vertigo, ataxia, dysarthria, dysphasia, hemi/quadriplegia
what to ask for a headache (red flags)?
SOCRATES, red flags = >60yrs, thunderclap, infective, hx malignancy
what to ask for weakness (red flags)?
SOCRATES, red flags = loss of sphincter control [spine problem like cancer, trauma, cauda equina syndrome], sudden onset [stroke], progressive, resp/swallowing problems
what to ask for visual disturbance (red flags)?
blur, monocular/binocular, diplopia, photophobia, speed of onset, pain in eye
what to ask for speech disturbance (red flags)?
confusion, dysarthria, dysphonia [laryngeal problems, resp muscle weakness], comprehension/receptive/wernickes, production/expressive/brocas, repetition [conductive dysphasia, arcuate fasciculus]
what to ask for dysphagia (red flags)?
neuro [bulbar and pseudobulbar palsy], mechanical (achalasia/stricture), solids/liquids, pain, nasal regurg, coughing, speed of onset), sensation (pain, odd distrubtion, +ve/-ve [numbness, paraesthesia], speed of onset
what to ask for blackouts (red flags)?
hx from pt/bystander, loss of consciousness, posture, provocation and prodrome, frequency, duration, tongue biting, incontinence, cyanosis, confusion after, shaking, chest pain, palpitations, fhx, driving
Indicators of raised ICP?
worsens when strain like coughing/sneezing, also have papilloedema, diplopia, difficulty concentrating
Symptoms from nox use?
B12 deficiency = paraesthesia, blindness, confusion, wernickes
What is hemiballismus?
one arm goes out and moves
5 tests to determine cognition?
AMT10 test, AVPU, MMSE, MOCA, ACE-R
What does the MOCA test?
for the younger population like PD; short term memory, visuospatial, attention, conc, working memory, language and time and place orientation
What is intranuclear ophthalmoplegia?
when nystagmus means eyes can’t communicate with each to move to look together at something
Bell’s palsy
can’t close the eye; affected side cannot move/show expression
Describing CT head?
patient demographics, type of scan (non-contrast CT), what plane the scan is in, describe what see (e.g. high attenuation lesion, left hemisphere, midline if centred or not), describe lesion; attenuation means area of colour different to what it should be (high = white, iso = middle tone and low = dark); extra/intra axial (inside or outside the brain when on an axial plane)
Causes for ischaemic stroke?
hypoperfusion, thrombus, embolus, cerebral venous sinus thrombosis
treatment options for ischaemic stroke (pharma)?
aspirin as prevention (300mg 2wks then long-term anticoag [clopidogrel or dipyridamole]); thrombolysis/thrombectomy (alteplase; check Cis, best within 90mins)
Types of ischaemic stroke?
total anterior circ infarct, partial anterior, lacunar (basal ganglia, internal capsule, thalamus [consciousness impaired], pons; ataxic hemiparesis, pure motor/sensory/both, dysphasia), posterior
S+Ss of stroke?
facial weakness, arm drift, abnormal speech, eyes deviate to the side of the lesion; if spinothalamic/corticospinal/dorsal column affected then hemiplegia, facial weakness, numbness, reduced sensation, reduced muscle tone, spasticity, hyperreflexia, weakness in tongue and sternocleidomastoid, carotid bruit; brainstem affects CNs (locked in syndrome)
cerebral cortex stroke?
aphasia, dysarthria, apraxia, visual field deficit, memory loss
cerebellar stroke?
ataxia, co-ordination, vertigo
ischaemic stroke risks?
stimulants, sickle cell, air pollution, MI, arrhythmias, cerebral venous sinus thrombosis (increase venous pressure exceeding arterial pressure), >45yrs, men
treatment for venous sinus stroke?
LMW heparin and then warfarin
TIA S+Ss?
cerebral ischaemia symptoms lasting <24hours; can get amaurosis fugax and less severe symptoms of stroke
TIA management?
ABCD2; stop driving for month
Management for stroke (not treatment)?
protect airway; bg 4-11mmol/L, bp only if thrombolysis; nbm until screen swallow, CT/MRI in 1hour if unusual/thrombolysis/haemorrhagic, otherwise 24hours
Causes of haemorrhagic stroke?
SAH/cerebral haemorrhage; from cerebral amyloid angiopathy, cerebral AV malformation, intracranial aneurysm
Management and treatment of haemorrhagic stroke?
bloods, CT head, stop anticoag/antiplatelet etc, ICPDs (the compressive squeezing leg stockings), reverse with vit K and beriplex (beriplex is faster acting for warfarin), aggressive bp control (140-160mmHg)
What is neuroplasticity?
part of brain dies their function is taken over by other part of the brain
Stroke investigations?
hypertension, 24 our ECG for AF, vasculitis, prothrombotic states, hypo/hyperglycaemic, thrombocytopenia, hyperviscous, genetics, carotid artery stenosis with carotid doppler/MRI
Stroke complications?
high ICP, low GCS when HTN, aspiration pneumonia (ng feed), pressure sores, depression, cognitive impairment
What does CHADSVASC stand for (when to treat with AF)?
Congestive heart failure, Hypertension, Age ≥ 75 (2), Age 65-74, Diabetes mellitus, Stroke/TIA/thrombo-embolism (2), Vascular disease, Sex Female
What does HASBLED stand for (warfarin or DOAC)?
Hypertension, Abnormal liver function, Abnormal renal function, Stroke, Bleeding, Labile INRs, Elderly (Age >65), Drugs, Alcohol use ≥ 8u / week
Hx for muscle weakness?
onset, proximal/distal, progressive, predisposing events, SOCRATES, symmetrical or not, local or diffuse, pain/motor/sensory, sphincter control, deformity, swelling, stiff, loss of movement/function; MRC grading
S+Ss UMN?
bulk normal, tone high, strength low, no fasciculations, high reflexes; corticospinal/pyramidal tracts (contralateral); groups of muscles; spasticity in stronger muscles (leg extensors and arm flexors); Babinski reflexes and clonus positive
S+Ss LMN?
reduced bulk, normal/decreased tone, low strength, may have fasciculations, low or no reflexes; anywhere distal to anterior horn (nerve roots, plexuses, peripheral)
What do the peripheral small nerves transmit?
pain and temp along spinothalamic tracts
What do the peripheral large nerves transmit?
proprioception and vibration
Common weakness causes?
steroid myopathy, statin myopathy, metabolic and endocrine, myotonic dystrophy, UMN/LMN, hypocalcaemia, hypokalaemia, anaemia, post viral, malignancy, infection, low CO, Guillain-Barre
Why would CK be raised?
inflammatory/proximal myopathy and anterior horn cell disease
S+Ss in weakness?
stairs, chairs, hair; wasting; facial weakness; neck weakness; contractures; scoliosis (Duchenne); eye movements rare
S+Ss in peripheral neuropathy?
chronic and slow progressing, sensory/motor/both, trophic changes (dryness, thin skin, deformity of nails, hair loss, ulcers), large fibre is more numbness and small fibre is more painful and burning sensation, ataxia, numbness, muscle wasting, paraesthesia
Causes of peripheral neuropathy?
Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, hereditary sensorimotor neuropathies (charcot-marie-tooth), diphtheria, porphyria are all motor; B12 and folate lack, diabetes, alcohol/drugs, metabolic abnormalities, leprosy, amyloidosis are sensory
What is mononeuritis multiplex?
painful, asymmetrical, motor; subacute; inflammatory mediated
What can cause mononeuritis multiplex?
vasculitides like churg strauss, connective tissue like sarcoid; ischaemic infarction of vasa nervosum from vasculitis
Median nerve (C6-T1) control?
controls LOAF (lumbricals, opponens, policis, abductor pollicis brevis, flexor policis brevis)
Ulnar nerve (C7-T1) control?
can’t cross fingers, weakness of medial flexors, medial 2 lumbricals (claw hand)
Radial nerve (C5-T1) control?
opens fist, BEAST (brachioradialis, extensors, abductor pollicis longus, supinator, triceps)
Brachial plexus S+Ss damage?
pain/paraesthesia along arm
Phrenic nerve (C3-5) S+Ss damage?
orthopnoea
Lateral cutaneous nerve of the thigh S+Ss damage?
anterolateral burning thigh pain
Sciatic S+Ss damage?
affect hamstring and all muscles and senses below knee
Common peroneal damage S+Ss?
foot drop, weak ankle dorsiflexion, sensory loss over foot dorsum
Tibial nerve damage S+Ss?
can’t stand on tiptoes, invert foot, flex toes, sensory loss on sole
Investigations for neuropathies?
Neuro screen, vasculitic screen, EMG/NCS, CSF, nerve biopsy
Treatment and management for neuropathies?
gabapentin/pregabalin/amitriptyline; remove underlying cause; prednisolone if inflammatory or vasculitis
Guillain Barre pathophysiology?
• AI against myelin (T cells and macrophages or IgG if axonal); post infection
Common GBS post infections?
resp/GI –campylobacter jejuni, flu, EBV, cytomegalovirus, varicella zoster, herpes simplex, zika
GBS S+Ss?
numbness distally, ascending weakness (1/2 day – 2wks to be max), paraesthesia, bifacial weakness, cranial neuropathies, areflexia, flaccid tetra/paraparesis
GBS investigations and results?
raised CSF protein, few cells; EMG slow nerve conduction; use IVIgs or plasmapheresis, DVT prophylaxis, BP, ECG, monitor swallow
GBS differentials?
spinal shock syndrome, botulism, myasthenia, lyme disease, toxins
GBS complications?
severe weakness, aspiration, resp failure, autonomic instability (monitor all of these – bp fluctuation and arrhythmia), hyporeflexia, ataxia, ophthalmoplegia, resp failure (breathing muscles failure)
Treatment for GBS?
ABCD, ABG, ECG, early anaesthesia, infection, supportive management of resp function, IVIg; improvement 2 days-6 months; LP (elevated protein); MRI, bloods; plasmapheresis
What is autonomic instability?
tachycardia, bradycardia, hyper/hypotension
Pathophysiology of myasthenia gravis?
• AI against nicotinic Ach receptors (abs = MuSK, LRP4)
MG S+Ss?
thymus dysfunction common (hyperplasia/thymoma); repetitive use of muscle = weakness shows; fatigueable weakness (proximal limbs, neck and face [head droop and ptosis], extraocular [complex diplopia], bulbar, speech); other AI diseases; no wasting/fasciculations; sensation, reflexes normal; dysphonia rare; reflexes normal
What population is mg common in?
3rd decade for women and 6th/7th for men
MG investigations?
tensilon test, achr abs (if -ve then NCS/EMG), EMG, CT thorax (thymoma), thyroid; if lift the ptosed eye then the other should ptose; anti-achr/anti-musk abs
MG treatment and management?
achesterase inhibitors (pyridostigmine – stop ach breakdown at NMJ), immunosuppressants (steroids, azathioprine/methotrexate/mycophenolate), thymectomy, stop antispasmodics/muscle relaxants, assess severity, bone protection (PPI), IVIg (for crisis), treat infections early and aggressively with abx; for severe generalised used rituximab
What can trigger myasthenic crisis?
infection, over/underdosing, abx/antiarrhythmics/beta blockers, disease progression, emotions, hypokalaemia, pregnant
How to manage myasthenic crisis?
review and think about breathing and monitor
Pathophysiology of MND?
• Degeneration of MN in motor cortex and anterior horns of spine
MND investigations?
LP, NCS/EMG/MRI
What is UMN only MND?
primary lateral sclerosis
What is LMN only MND?
primary muscular atrophy
What is both L and UMN MND?
amyotrophic lateral sclerosis
What is bulbar only MND?
progressive bulbar palsy
MND S+Ss?
asymmetrical weakness; bulbar/limb onset; no sensory/visual/BB; 2-5yrs survive; UMN is pyramidal signs (spastic, increased tone, hyperreflexive, weakness), LMN (flaccid dysarthria, loss of tone, loss of reflexes, weakness); >40yrs, stumbling spastic gait, foot drop, proximal myopathy, weak grip, should abduction and sometimes aspiration pneumonia
What is MND diagnosis from?
clinical supported by electrophysiology; sensory should be normal in NCS, motor can be normal (as compensatory innervation can make up for the loss) or abnormal; Awaji-Shima criteria for ALS (give EMG findings [fasciculations, fibrillations] for active denervation with re-innervation as much weighting as clinical findings; need at least two muscles that this is true for)
MND differentials?
radiculopathy, CIDP, myopathy, MG
What is MND treatment and management?
MDT, riluzole (inhibits glutamate release and NMDA receptor antagonist); antimuscarinic for stop drooling; blend food for dysphagia; exercise; palliative; find way of communicating effectively
What can cause a coma?
drugs, anoxia, mass lesions, injury, infections, infarcts, metabolic, epilepsy, SAH, sometimes psych, hypothermia, venous sinus occlusions, tumour; hx, previous events, suicide attempts, travel
What does GCS assess?
eye, motor and verbal in consciousness
What exams are needed in assessing coma?
trauma, skull, fever, hypothermia, breath odour, needle marks, liver disease, convulsion, alert bracelet, skin colour, GCS (may not be able to maintain airway), eye reactions, focal deficits, meningism, bp, pulse, emergency bracelet, resp/carido/neuro/abdo
What investigations are needed in assessing coma?
bloods, imaging, LP, EEG
What S+Ss for cocaine use?
seizures, tic-like movements, crack is anxiety, confusion, paranoia, visual hallucinations, psychosis, stroke
What is status epilepticus?
persistent seizure activity for 30 mins+ either continuous or intermittent without recovery
Causes of status epilepticus in adults?
usually anticonvulsant/alcohol withdrawal (pabrinex or thiamine), cerebrovascular disease, metabolic disorders (lactic acidosis, high K+, sugar, CO2, low Na), renal, autonomic (hyperpyrexia, failure of cerebral autoreg, vomiting, incontinence), CVA
Assessment of status epilepticus?
rule out infection with LP, CT, EEG when less obvious to diagnose, O2, cardiac and resp assess, blood glucose
Emergency treatment of status epilepticus?
IV benzodiazepine (midazolam/diazepam rectal if can’t swallow – give IV phenobarbital after trying IV lorazepam) fit more than 5 mins, if no work then give antiepileptic drug IV (phenytoin, levetiracetam, sodium valproate, phenobarbital), if this doesn’t work then general anaesthesia and intubation
Sudden onset headache causes?
SAH, cerebral venous thrombosis, dissection carotid/vertebral, bacterial meningitis, encephalitis, cerebral abscess, acute haemorrhage
SAH S+Ss?
thunderclap, dizzy, vomiting profusely, ptosis, eye movements painful, pupillary reflexes normal, stiff neck, photophobia, spontaneous onset, low GCS, 3rd CN palsy
SAH treatment?
surgical clipping or endovascular coiling
Sudden onset headache investigations?
CT (better closer to event), MRI, LP (xanthochromia 12hours to 2wks after – yellow CSF)
Two types of acute neuropathies?
acute demyelinating or motor axonal
Acute neuropathy S+Ss?
peripheral paraesthesia then pain, then starting to fall even if early 30s from weakness
Acute neuropathy investigations?
NCS
Investigations for transient LOC?
12 lead ECG, CT head, EEG, home recording, bloods
Pathophysiology of epilepsy?
clinical manifestation of abnormal and excessive discharge of cerebral neurones, resistance of excitatory neurones firing in refractory period is decreased; upregulation of excitatory circuits and down-regulation of inhibitory, brain structure may have changed, failure of GABA neurotransmission, if epileptic then tendency to unprovoked seizures
Epilepsy PMH?
childhood development, head injury, neurosurgery, stroke, malignancy, AI, neurodegenerative, LD, drugs, metabolic disorders
Epilepsy S+Ss?
simple/complex partial seizures (simple = aura) or generalised tonic clonic (may have aura, stiffen, jerk, grunting, cyanosis, eyes open, 1-2mins, 20mins post-ictal confusion/headache or 1-2 hours, lateral tongue biting, urinary incontinence, injury), myoclonic jerks, absences (SEE PHASE 2A NOTES, brief and appear to drift off), without warning, loss of awareness, awake/asleep, childhood/teenage onset, aura, focal motor activity, automatisms, epigastric sensations, nausea, abnormal taste/smell, SUDEP (most common cause of death)
Common epilepsy triggers?
early morning, sleep deprivation, alcohol, photosensitivity; tramadol
DVLA notification for epilepsy?
car 6 months and 12 months after, HGV 5 years then 10 years
Epilepsy tests?
EEG, MRI, ECG, 3-12 month review
Treatment and management of epilepsy?
= AEDs, levetiracetam (most commonly used), lamotrigine, valproate (not used for women of childbearing age - teratogenic), lots of SEs common, adjunctives = clozabam, topiramate, focal use carbamezapine/levetricetam/lamotrigine
What is complex epilepsy and how is it treated?
not controlled for 2 years, unsuccessful with 2 AEDs, bad SEs from AEDs, psych comorbidity, unilateral structural lesion; vagal nerve stimulation, surgery for refractive focal epilepsy (anterior/medial temporal lobe resection), SUDEP in uncontrolled
Whats is syncope from transient global hypoperfusion?
from lack of blood/oxygen flow to the brain so loss of oxygen
What is reflex syncope and causes?
neural – vasovagal from emotion/pain/standing, situational [cough, effort, micturition] from sneeze, carotid sinus hypersensitivity from head turning
What is cardiogenic syncope and causes?
Wolff-Parkinson-white, bruguda syndrome, arrhythmogenic right ventricular dysplasia; fewer prodrome symptoms than the other causes of syncope; Stokes Adams attacks
What is orthostatic hypotension and its causes?
drugs, autonomic failure, hypovolaemia, PD, diabetes, MSA
What is neurogenic syncope and its causes?
inappropriate activation of PNS [vagal nerve] and decrease of SNS
Give the different types of syncope?
anxiety, factitious (Munchausens), hypoglycaemia; when vessels don’t constrict to bring blood flow to brain when stand up), structural cardiac disease, cerebrovascular, substance abuse, psychogenic (panic attacks), reflex, cardiogenic, neurogenic and orthostatic
PMH of syncope?
previous faints, poor oral intake, PMH
Syncope S+Ss?
prodrome = hot, dizzy, visual crowding, ear ringing, pale; S+Ss = pallor during, brief, jerks if upright, fainting prodrome, loss of consciousness ask, <20 secs to some minutes, nausea, sweating, blurred vision, chest pain, dyspnoea, palps, recovery v quick
Syncope investigations?
don’t need CT, triggers, change in med, postural tone loss, sudden death, 24 hour tape, tilt table, autonomic function tests; ECG, ECHO
What is a psychogenic non-epileptic seizure (NEAD)?
– appears like epileptic but no ictal cerebral discharges; from psych distress (childhood sexual abuse or just stress); may have epilepsy as well
Differentials of a NEAD?
hypoglycaemia/acute hydrocephalus, never really think about TIA
Difference in hx of NEAD to epilepsy?
no urinary incontinence/tongue biting/tonic clonic movements/unexplained anxiety/deja vue
PMH of NEAD?
birth, febrile seizures, CNS infections/head injuries, psych problems; DH = antidepressants and tramadol; SH = psych, alcohol, drugs, driving, psychosocial
NEAD S+Ss?
subjective symptoms, eyes usually closed, partially responsive, wax and waning symptoms, emotional, long, tired and washed out post-ictal, random but gradual onset, awake or asleep, over 2 mins, violent thrashing, side to side head, asynchronous movements, may have aura and partner may be aware
NEAD treatment and management?
neuropsychotherapy and don’t give anti-epileptics
Causes of unilateral vision loss?
vascular (amaurosis fugax, central retinal vein occlusion, anterior ischaemic optic neuropathy), optic neuritis, retinal detachment, vitreous haemorrhage, acute angle closure glaucoma
What is central retinal vein occlusion and some S+Ss?
cotton wool spots, multiple retinal haemorrhages, pale optic disc, cherry red spot in macula, ocular equivalent of a stroke
What is an anterior ischaemic optic neuropathy?
posterior ciliary artery occluded, supplies optic nerve head, papillodema] - GCA
What happens with a retina detachment?
flashes/floaters with decrease in vision, retina peeled away, curtain covering vision, surgical repair
S+Ss of vitreous haemorrhage?
flashes/floaters with low vision with diabetic retinopathy, red tinge from blood, blurred vision, visual loss
S+Ss acute angle closure glaucoma?
painful red eye with N+V, treat with bright room
Treatment acute angle closure glaucoma?
pilocarpine [constricts pupil] or timolol drops [beta blocker], surgery/laser treatment
Loss of vision investigations?
hx and exam, visual evoked potential/MRI, fluorescein angiography, tonometry (for glaucoma in eye pressure), US
What is a clinically isolated symptom?
first episode of symptoms from inflammatory demyelination
Normal ophthalmoscopy?
macula, optic nerve and photo orientation mark
Abnormal ophthalmoscopy?
if inflamed optic nerve head (papillitis) but behind nerve is normal; swollen optic disc = anterior ischaemic optic neuropathy; central retinal artery occlusion = cherry red spot at macula; central retinal vein occlusion = dilation of branch veins, cotton wool patches and multiple retinal haemorrhages
MS pathophysiology?
lesions in CNS (white matter in optic nerve, brainstem, basal ganglia and spinal cord – at least 2+ and 30 days or more between attacks), inflammation and destruction of myelin; loss of oligodendrocytes means myelin loss and progresses to axonal loss; remyelination at first but less successful as progresses; more astrocytes as neurone loss; inflammation from T cells
MS associations?
EBV and herpes simplex, smoking, stress and diet
MS S+Ss?
blindness/hemianopia, optic neuritis (reduced/loss of vision in eye), diplopia, horizontal nystagmus, lateral rectal weakness, facial weakness (pain bursts, cough, hiccough, paraesthesia, complex gaze palsies), sometimes deafness, acute demyelination in brainstem means positional vertigo, ataxia, vomiting, visual auditory attention loss, amnesia, depression, damage in posterior column of cervical cord (tightness, burning, pulling, twisting, tearing), loss of thermal/pain sensation, loss of leg sensation (triad associated with cauda equina), impotence in men, loss of thermoregulation, UMN signs (spastic and brisk reflexes), optic atrophy, cerebellar signs, internuclear ophthalmoplegia, dysarthria, incontinence, L’Hermitte’s, worse with heat
MS tests?
MRI gives high T2 signal lesions in white matter (mainly periventricular)
MS diagnosis?
presence of multiple CNS lesions, symptoms longer than 24 hours and disseminated in time and space (>1 month apart); relapses from viral infections, stress; McDonald criteria; 4 types = relapsing/remitting, secondary progressive (after RR), primary progressive and progressive remitting
MS treatment?
amantadine for fatigue, exercise, baclofen/gabapentin for spasticity, amitriptyline for emotions, for relapses give oral methylprednisolone for 5 days; interferon beta 1a/1b (disease modifying)
Optic neuritis causes?
= acute demyelinating, ischaemic optic neuropathy, corticosteroid responsive (AI), post infection, post vaccination, infections, vitamin B12 low, drugs (amiodarone, ethambutol), viral infection in kids
Optic neuritis S+Ss?
triad of visual impairment (worsened by hot shower), pain around eye (worsened by movement), impairment of colour vision, others = light flashes, Uhthoff’s phenomenon (body gets overheated in demyelinating – hot weather, hot tubs etc), Pulfrich’s phenomenon (still target moves in ellipsis laterally), fatigue, decreased pupillary light reaction, arcuate defects, scotoma, RAPD, dyschromatopsia (loss of colour vision)
Optic neuritis treatment?
refer to ophthalmologist/neurologist, methylprednisolone in acute, MRI, neuro assessment, normally resolves on its own or sometimes with steroids, 6wk recovery, risk increased for developing MS
Neuromuscular emergencies?
- Swallowing – if structural then liquids ok until disease progresses but neural is if both solids and liquids from onset
- MND – speech precedes swallowing problems (RED FLAG)
- MANAGEMENT – abcd, ABGs, early anaesthetic help, infection?, treat underlying cause
- Type 2 resp failure – from respiratory muscle failure (MG – myasthenic crisis)
Proximal myopathy S+Ss and causes?
affects hair, stairs and chairs, not reflexes, specific muscles, not paraesthesia/bladder weakness; kids = Duchenne muscular dystrophy, adults from corticosteroids use
Neuromuscular syndromes S+Ss and causes?
fatigable, repeatable; writing, walking, brushing teeth; MG, Lambert-Eaton (defective ach release at presynaptic nerve so proximal muscle weakness [voltage gated calcium channels], extraocular/bulbar not usually involved, can have bilateral partial ptosis
Neuromuscular syndromes treatments?
corticosteroids and immunosuppressants [pyridostigmine and IVIg])
Peripheral neuropathy types and S+Ss?
large fibre = signs seen before symptoms; small fibre = pain and burning in feet at night; trophic changes (shiny skin, loss of hair, dryness and nail changes)
Radiculopathy causes, areas and S+Ss?
usually C6-7 (bicep/tricep wasting) and L5-S1 (L5 dorsiflexion and S1 plantar flexion); sciatic from spinal degeneration and nagging pain (more shooting and sharp) with numbness and weakness; pancoasts tumour = ulnar radiculopathy in smokers; cauda equina syndrome (incontinence, saddle paraesthesia); spinal claudication (pain down one or both legs only with walking – easy to treat)
Vertebral pain syndrome S+Ss?
aching, nagging pain isolated to before joint, arthritic; relieved by rubbing and heat; paraesthesia, weakness and numbness, reduced ROM
Myelopathy S+Ss?
spinal cord; signs before symptoms; UMN (Babinski, clonus, loss of fine motor movements, Hoffman’s, hyperreflexia, cross adductors and deltoid/pectoral reflex)
Cavernous sinus syndrome S+Ss?
CN 3, 4, 5, 6 palsies
Spinal claudication causes?
canal stenosis or cauda equina syndrome
What syndromes cause nerve thickening?
Charcot-Marie-Tooth or leprosy
What does an EMG do?
record electrical activity of skeletal muscle; diagnosis for neuromuscular/motor control diseases; assesses fasciculations and voluntary movements
What can EMG be used for assessing?
neurogenic disorders (see gaps between interference indicating axonal loss and see tiny little discharges/fibrillations between this, also see this in myopathy; fibrillations are always pathological); myopathy (full and early motor activation, low amplitude); myotonia (wax and wane in spontaneous firing, in muscle fibre membrane channelopathies); use single fibre for looking for NMJ disorders
What does NCS do?
evaluates function and ability of electrical conduction of sensory/motor nerves
What types of NCS are there?
motor and sensory (peripheral nerve stimulation), F-wave study (supramaximal stimulation of a motor nerve and record action potentials sent to its muscle) and H-reflex study (stimulation of nerve and record reflex electricity in muscle in limb)
When is a brain biopsy needed?
for tumour, infection and inflammation diagnosis; stereotactic brain needle biopsy (small hole into skull and needle guided by CT/MRI), scar can cause seizures
When is a muscle biopsy needed?
for distinguishing myopathy from neuropathy in weakness and low muscle tone
When is a nerve biopsy needed?
indicate damage to myelin sheath, damage to small nerves, axonal destruction and neuropathies
What is a GCA score for?
• Level of consciousness in those with trauma brain injury
What is abnormal, moderate and severe from a GCA score?
3-14 abnormal (moderate = 9-12 and 8 or below is severe)
When is an angiography used?
aneurysms, stenosis, atherosclerosis, vasculitis, AV malformation, thrombosis and vasospasm
What are angiography SEs?
TIA, loss of consciousness and hemiplegia
When is an LP used?
= meningitis, SAH, hydrocephalus, benign intracranial hypertension, medulloblastoma, inject meds (spinal anaesthesia, chemo)
LP complications?
headache, nausea responding to analgesia and fluids, paraesthesia
What may increased CSF pressure in LP mean?
congestive HF, cerebral oedema, SAH, meningeal inflammation, hydrocephalus
What may decreased CSF pressure in LP mean?
subarachnoid blockage, severe dehydration, hyperosmolality; pleocytosis (WBC presence – leukaemia, mets, recurrent epileptic seizures)
What may granulocytes in LP mean?
Bacterial meningitis
What may RBCs in LP mean?
intracranial haemorrhage
What may low glucose in LP mean?
lymphoma, leukaemia, fungal TB
What may high lactate in LP mean?
CNS cancer, MS, traumatic brain injury, brain abscess, hydrocephalus, resp alkalosis
What may high protein in LP mean?
spinal block
What may oligoclonal bands in LP mean?
MS
When is a spine/brain MRI used?
• For tumours, abscesses, congenital abnormalities, aneurysms, venous malformation, haemorrhage, subdural haematoma, MS, encephalomyelitis, herniated discs, spinal cord compression
When is an MRI contraindicated?
pacemakers, cochlear implants, implanted drug infusion pumps, metal implants
What is a T1 and T2 MRI?
T1 = CSF dark and for anatomy, T2 = CSF light and white matter dark so useful for pathology
What is a FLAIR MRI?
white matter plaques for seeing demyelination
When is a CT head most useful for?
Trauma and spiral for kids who can’t keep still
Other uses for CT head?
intracranial haematomas, brain contusions, oedema, foreign bodies, brain injury, haemorrhage, stroke, tumours, hydrocephalus, disease, skull malformation
What is an EEG?
Non-invasive testing electrical activity in the brain (voltage fluctuations)
What is an EEG for?
epilepsy (sometimes during seizure – localise it and distinguish from others), sleep disorders, coma, encephalopathies, brain death, depth of anaesthesia, cerebral perfusion in endarterectomy, SAH brain damage
What is rhythmic activity in EEG?
divided by frequency; abnormal activity = epileptiform/non-epileptiform, focal (can identify area of cortical irritation during seizure)/diffuse (more for generalised epilepsy)
What are transients in an EEG?
spikes and are abnormal and can be epileptiform (that identify epilepsy)
Pathophysiology of Huntington’s?
• Progressive, neurodegenerative from CAG repeat on 4q, AD inheritance; more glutamines so huntingtin accumulates in neurones of dorsal striatum and caudate nucleus
HD S+Ss?
(30-50yrs onset) = chorea (involuntary movements – peaks and declines, worsened by stress/anxiety/depression), impairment of voluntary, akathisia (feeling restless), rigidity and spasticity later unless childhood onset (can get myoclonus), bradykinesia, dysphagia later (can be cause of death – aspiration, weight loss), dysarthria, falls common, incontinent, sleep disturbance, lose driving ability; cognitive = disruption in planning, organisation, lack of initiative, perseveration, impulsivity, irritable, temper, low spatial perception, low self-awareness, difficulty learning new, lack of time awareness; psych = depression, mania, anxiety, apathy, delirium, sexual disorders, OCD
HD treatment and management?
supressing chorea (neuroleptics like haloperidol, fluthenazine; benzodiazepines; dopamine depleting agents like tetrabenazine and reserpine but they do have SEs and see psych crib sheet, can worsen dysarthria), relieving stiffness (benzodiazepines but can cause bradykinesia), reliving spasticity (tizanidine = alpha2 agonist), antiparkinsonian meds for rigidity and bradykinesia; other management = PEG feeds for dysphagia, calorie content assessed, hydration and maybe puree food