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
Parkinson’s pathophysiology?
low dopamine in pars compacta of substantia nigra; circuits to basal ganglia affected = motor, oculo-motor, limbic, orbitofrontal; can be from alpha-synuclein bound to ubiquitin in damaged cells (Lewy body – in olfactory bulb, medulla oblongata, pontine at first)
Risk factors for PD?
genes like PARK 1, 4, 5; heavy metals; pesticides; FH; 2nd most common neurodegenerative disease; 7-14 years expectancy
PD S+Ss?
primary parkinsonism; motor with autonomic dysfunction/neuropsych/sleep disturbance; 4 main symptoms = tremor (at rest not in sleep/voluntary movement pill rolling), rigidity (cog wheel/lead pipe neck and shoulders first), bradykinesia (start with fine motor), postural instability; others = fast shuffling and forward flexed gait, asymmetrical arm swing; cognitive in early disease (memory affected like recalling, dementia); mood difficulty (depression, anxiety, apathy); low facial expressions; quiet speech; hallucinations/delusions; sleep problems, orthostatic hypotension, constipation, vision abnormal, impaired smell and pain sense; other symptoms = progressive supranuclear palsy, multiple system atrophy, cortico-basal degeneration, lewy body dementia
PD diagnosis?
on hx and examination and rule out PSP and multiple system atrophy; CT/MRI
PD treatment and management?
no cure; levodopa dopamine analogue standard used 30mins before meals but later in disease gives motor complications like chorea (also in diagnostic stages to see if improves with it); carbidopa and benserazide are peripheral dopa decarboxylase inhibitors; tolcapone inhibits COMT breaking down dopamine; bromocriptine and pramipexole are dopamine agonists (similar to levodopa); selegiline and rasagiline are MAO-B inhibitors that block dopamine metabolism in basal ganglia; amantadine for motor symptoms; exercise programmes; dysphagia so use thickeners; MDT
Causes and red flags of an acute headache?
hx of cancer; above 50yrs (GCA, mets, temporal arteritis); thunderclap/worst ever/vomit at onset (SAH [LP after 12 hours if CT head negative and still suspect but not valid after 12 days, can look for aneurysm after this time using CT angiography], can also get cerebral vasoconstrictive syndrome [from drugs like sumatriptan or over the counter]); meningism (LP, kernigs, Brudzinski, fever, tachycardia, non-blanching rash, CRP); raised ICP signs (worse in morning, papilloedema can eventually get tunnel vision [can look like optic neuritis from MS which is more diffuse headache with pain on movement and visual changes early (scotoma); also look like diabetic papillitis], worse on straining/leaning forward, vomiting; pressure from LP pressure over 30 is abnormal, 14 is normal); idiopathic intracranial hypertension and normal pressure hypertension can cause blindness (losing weight can help, surgery); medication (GTN, nitrates, omeprazole); sleep apnoea (worse in morning); hypertension; sinusitis (can be worse in morning); psychogenic (worse in morning too)
Differentiating between migraine and TIA?
migraine more +ve symptoms; more tingling than numbness in migraine; aura in migraine but usually hemianopia in TIA; more weakness with TIA; sudden onset with TIA and migraine more gradual
Temporal arteritis S+Ss and risks?
scalp tenderness; risk of amaurosis fugax (TIA of posterior ciliary artery) and posterior circulation stroke
What is a chronic headache?
more than 3 months
Causes of chronic headache?
migraine and chronic daily syndrome headaches (medication overuse – rebound headaches from stopping it)
Migraine prevention and acute treatment?
prevention = propranolol 1st line, 2nd line tricyclics, topiramate 3rd line, 4th line candesartan or valproate if no contraindication; for acute = NSAID with triptan
What does DANISH stand for for cerebellar syndrome?
dysdiadochokinesia, dysmetria, ataxia, nystagmus, intention tremor, slurred speech, hypotonia
What side is affected in cerebellar syndrome?
Ipsilateral
Give an overview of peripheral neuroanatomy?
anterior horn, nerve, muscle; ventral roots are motor and dorsal is sensory
Give the controls of nerves C5, 6, 7, 8, T1 and 2?
Over deltoid, index finger, middle finger, little finger, inner arm, apex of axilla
Give the controls of nerves L2, 3, 4, 5, S1 and 2?
Anterior medial thigh, over the knee, medial aspect of tibia, dorsum of foot to big toe, lateral heel, popliteal fossa
winging scapular causes?
Long thoracic nerve = serratus anterior; Accessory = trapezius (uncommon); Dorsal scapular = rhomboids (rare)
What is progressive supranuclear palsy and what areas of the brain are affected?
• Gradual deterioration in specific volumes of the brain; neurofibrillary tangles seen; basal ganglia, brainstem, cerebral cortex, spinal cord, dentate nucleus affected; can have Pick’s disease
Progressive supranuclear palsy S+Ss?
loss of balance, bumping into objects, fast walking, personality change, bradykinesia, visual symptoms; later = dementia, dysarthria, dysphagia, difficulty moving eyes, neck stiffening, incontinence, constipation
Progressive supranuclear palsy treatment?
no cure; amantadine, levodopa for neck dystonia, rivastigmine for cognition
Progressive supranuclear palsy complications?
pneumonia (cause of death), Richardson syndrome (postural instability, supranuclear vertical gaze palsy, frontal dysfunction), PSP (asymmetrical tremor, initial levodopa response), infection
What is multiple system atrophy and what areas of the brain are affected?
• Neurodegenerative affecting substantia nigra, striatum, ANS; onset 50-60s; gliosis and astrocyte proliferation and Papp-Lantos bodies
What is multiple system atrophy S+Ss?
autonomic dysfunction, parkinsonism, ataxia; sometimes ED or postural hypotension; later sleep disorders, constipation, vocal cord paralysis, difficulty regulating body temp, sometimes cognitive impairment; no cure
Meningitis S+Ss?
severe headache, nuchal rigidity, sudden high fever, altered mental state, photophobia, phonophobia, Kernig’s, brudzinski’s sign, petechial rash, bulging fontanelles <6 months
Meninigitis complications?
sepsis, DIC, gangrene, focal seizure, CN abnormal
Meningitis causes?
viral (herpes simplex, VSV, HIV, mumps), bacterial, fungal, protozoa, sarcoidosis, SLE, malignant
Meninigitis risks?
HIV and immunosuppressants
Meningitis tests?
FBC/CRP/blood cultures, LP, hyponatraemia common in bacterial
Meningitis treatments?
prophylaxis for close contacts (rifampicin, ciprofloxacin, ceftriaxone); IV fluids, mechanical ventilation, third generation cephalosporins (ceftriaxone), meningococcal then use benzylpenicillin, if h.influenzae then use corticosteroids, viral supportive and acyclovir, fungal with amphotericin B
What is encephalitis?
• Sudden onset inflammation of brain
Encephalitis S+Ss?
acute fever, headache, confusion, seizures, irritable, poor appetite
Encephalitis causes?
viral = rabies, herpes simplex, polio, measles; bacterial = meningitis
Encephalitis tests?
MRI T2 hypersensitivity in median temporal, EEG, LP, bloods, urinalysis
Encephalitis treatment?
steroids reduce swelling, sedatives, antivirals/biotics
Brain tumour S+Ss?
high ICP, headaches, frontal lobes (poor reasoning, personality change, inappropriate social, poor planning, decreased speech), temporal (memory loss, hearing loss, difficulty in language comprehension), parietal (poor interpretation of languages, decreased pain sense, poor spatial/visual awareness), occipital (poor/loss vision), cerebellar (poor balance, muscle movement, posture), brainstem (bp, swallowing, heartbeat)
Primary brain tumours?
• Meningiomas benign; primary = glial cells (malignant); pituitary adenomas and nerve sheath
Brain tumour tests?
CT/MRI BBB disruption; EEG
Mets to become brain tumour?
lung, breast, malignant melanoma, kidney, colon
Brain tumour prognosis?
medullablastoma (good), glioblastoma multiforme (bad), oligodendrogliomas (incurable – slow progressing)
History for spinal cord injury?
• Traumatic or not; mechanical, toxic and ischaemic; level is lowest level of full sensation and function; complete is everything below level function lost; sensory exam = 0 for absent, 1 for impaired and 2 for normal
What is a romberg test for?
balance/proprioception; cerebellum, vestibulum
What does a pronator drift show?
pyramidal lesion, power
Cord compression causes?
canal stenosis, herniated discs, tumours (mets, astrocytoma, neurofibroma, meningioma)
Cord compression S+Ss?
bilateral leg weakness, bladder/anal sphincter giving hesitancy and frequency, look for motor, reflex and sensory level
Cord compression tests?
spinal MRI, biopsy, bloods, CXR
Cord compression treatments?
urgent dexamethasone with specific therapy for malignancy and drainage and abx for abscesses
Cord vascular problems causes?
epidural haemorrhage, spinal cord ischaemia (aortic dissection, aortic aneurysm repair, inferior venecal thrombosis)
Altered sensation from spinal cord causes?
peripheral neuropathy, CNS disorders (stroke/MS), nereve root lesions, spinal cord compression, hyperventilation, circ disturbance (Raynaud’s/PVD/embolic)
Inflammatory spinal cord injury causes?
acute transverse myelitis, neuromyelitis optica (spinal cord and optic nerve, brainstem, aquaporin-4 ab, longitudinal lesion in MRI)
Infection spinal cord injury causes?
abscess (bacteria/tuberculosis), herpes simplex, chronic meningitis, meningo vascular syphilis, cytomegalovirus, schistosomiasis
What is central cord syndrome and its S+Ss?
damage of cervical, weakness of arms, legs spared, spared sacral sensation; loss of pain, light touch and pressure below injury; usually from neck hyperextension in elderly with spinal stenosis
What is cervical spondylosis?
degeneration of annulus fibrosis ad osteophyte formation narrowing spinal cord and traps cord
Cervical spondylosis S+Ss?
neck stiffness, crepitus, brachialgia (arm pain), forearm/wrist pain, L/Hermitte’s, LMN signs if radiculopathy, UMN if cord compression
Cervical spondylosis management?
urgent MRI, specialist referral, if not urgent then analgesia and gentle activity; may need laminectomy/laminoplasty
What is anterior cord syndrome and its S+Ss?
anterior cord damage or reduction in supply to anterior cord; below level = motor, pain and temp sensation lost
What is Brown Sequard sydrome?
hemisection of spinal cord (loss of motor, proprioception, vibration ipsilateral, pain and temp loss contralateral)
What is posterior cord syndrome?
posterior spinal artery infarct; loss of proprioception, vibration
What is cauda equina syndrome and its S+Ss?
saddle paraesthesia, bowel disturbance, urinary incontinence, paraesthesia, spasticity, sexual dysfunction, leg weakness areflexic and flaccid, back pain and may radiate down legs; from conus medullaris syndrome, ruptured intervertebral disc, tumour, fecal impaction
Pathophysiology of neurosarcoidosis?
chronic, non-inflammatory; non-caseating granulomas in different parts of body, 10% of those with sarcoidosis
S+Ss of neurosarcoidosis?
cranial nerve abnormality (usually CN7), decrease in visual perception, seizures, meningitis, depression, psychosis, peripheral neuropathy, Sometimes dyspnoea, arthralgia, jaundice, HF
Neurosarcoidosis treatment?
prednisolone, immunosuppressants (methotrexate and cyclophosphamide)
What is muscular dystrophy?
Progressive weakness and muscle wasting
5 types of muscular dystrophy?
Duchenne, Becker’s, FSH, limb girdle, myotonic
Features of duchenne?
most progressive; FH, features, lab findings (mostly CK), myopathic EMG, muscle biopsy
Features of Becker?
More benign than duchenne
Features of facioscapulohumeral?
slow progressing of facial, scapular, humeral and peroneal; life expectancy normal and takes 10 yrs to show symptoms
Features of limb girdle?
hip and shoulder; 20-30years onset; cardiac and resp symptoms
Features of myotonic?
AD inheritance; facial and distal muscle weakness/wasting, myotonia (tonic muscle spasm), frontal balding, cataracts, pulmonary hypoventilation, mild mental retardation; can use mexiletine
Common causes of movement disorders?
PD (rest or re-emergent), benign essential tremor (postural), drug induced (alcohol, neuroleptics, beta agonists), thyrotoxicosis, intention usually from cerebellar
Less common movement disorder causes?
Huntington’s, chorea, liver failure, tics/jerks/spasms, cerebellar disorder, wilson’s
Wilson’s S+Ss?
asymmetrical and variable tremor, difficulty speaking, excess salivation, ataxia, clumsy hands, personality changes, high copper, kayser-fleischer rings, caeruloplasmin used to treat
Essential tremor causes?
action, postural; onset after 65 with cognitive impairment
Essential tremor management and treatment?
avoid caffeine/stress; use beta blocker (propranolol)
What is hemiballismus?
proximal hemichorea contralateral to lesion in subthalamic nucleus; recovers spontaneously over months
What is athetosis?
slow, repetitive, purposeless movements; mainly from cerebral palsy but if pseudoathetosis from severe proprioceptive loss
What is myoclonus?
sudden involuntary focal or general jerks from cord, brainstem or cerebral cortex; can have asterixis in wrists from liver/kidney problems; can also have benign essential myoclonus
What is a tardive syndrome?
twisting and choreiform movements of proximal/trunk muscles from dopamine antagonists
How is a tardive syndrome treated?
Treat with tetrabenazine and withdraw drugs in question
What is dystonia?
prolonged muscle contractions causing abnormal posture
Types of dystonia?
Idiopathic general, focal and acute
How to treat general dystonia?
anticholinergics and muscle relaxants
How to treat focal dystonia?
inject with botox
How to treat acute dystonia?
neuroleptics and some anti-emetics like metoclopramide and cyclizine if from drugs
Some complications from acute dystonia?
torticollis [head pulled back], trismus [oropharyngeal spasm] and oculogyric spasm [eyes drawn up]
Common causes of abnormal gait?
stroke, childhood hip disorders, PD, cerebral palsy, MS, spinal cord compression, joint disorders
Uncommon causes of abnormal gait?
cerebellar problems, peripheral neuropathies, myopathies, GBS, polio, MND
What is spastic gait?
stiff, circumduction of legs
What causes spastic gait?
UMN lesions
What is extrapyramidal gait?
flexed posture, shuffling feet, postural instability
What causes extrapyramidal gait?
PD
What causes steppage gait?
foot drop from MS, GBS, peroneal nerve injured, prolapsed intervertebral disc
What causes difficulty turning?
Cerebral/basal ganglia
What is myopathic gait?
waddling, can’t stand from sitting, cannot climb stairs; hip girdle weakness
What is psychogenic gait?
doesn’t follow any other gait disorder pattern
What is ataxic gait and causes?
looks like a novice on an ice rink (widened base and unsteady); multi-infarct states and normal pressure hydrocephalus
What causes frontal gait disorder and what is it?
cerebral tumours, subdural haemorrhage, hydrocephalus, multiple lacunar infarcts; slow, shuffling, wide, hesitation, poor posture
What is paraparesis?
bilateral leg weakness and hyperreflexia
What is scissor gait?
spastic cerebral palsy
What is trendelenburg gait?
hip abductor weakness/pain and L5 radiculopathy
Common causes of vertigo?
benign positional vertigo, Meniere’s, vestibular neuronitis, brainstem stroke, postural hypotension
Uncommon causes of vertigo?
arrhythmia and MS; o Ototoxicity = aminoglycosides, loop diuretics, cisplatin
o Acoustic neuroma = schwannoma from vestibular nerve, unilateral hearing loss and vertigo later, slow growing
o Trauma = petrous temporal bone, cerebellopontine angle affected then can interfere with auditory nerve
o Herpes zoster = if erupts over external auditory meatus
Questions to ask pt for vertigo?
vertigo, disequilibrium, presyncope, lightheaded
What is a benign paroxysmal positional vertigo (BPPV)?
detached otoliths in utricles and saccules when head stopped moving so vertigo
What are causes of BPPV?
idiopathic, head injury, spontaneous degeneration of labyrinth, post viral, post-stapes surgery, chronic middle ear disease
What RFs are there for BPPV?
older (50yrs), women, Meniere’s, anxiety, migraine
BPPV S+Ss?
worse on head movement (side to side), sudden onset attacks 20-30secs, nausea, worse in morning, hearing unaffected
Examinations for BPPV?
= ear drum, CNs, Dix-Hallpike test (should see nystagmus)
BPPV red flags?
unilateral hearing loss, new onset headache, focal neuro signs, atypical nystagmus, cerebellar signs
BPPV treatment and management?
reassure that resolves and 50% recur, Epley’s manoeuvre
What is menieres?
disorder of inner ear from change in volume in labyrinth
RFs for menieres?
allergy, AI, genetics, Na/K disturbance, vascular, viral infection, 40-60yrs
Menieres S+Ss?
vertigo, tinnitus, fluctuating hearing loss, aural pressure sense, attacks 2-3 hours and in clusters, start off unilateral, some unexplained falls, earlier = vertigo attacks more common and loner remission but then middle stage = vertigo with pre-giddiness and sensorineural hearing loss and tinnitus worse, late = vertigo less, hearing loss worse
Menieres tests?
CNs, ears, cervical spine, Hallpike manoeuvre, exclude: other ENT, intracranial, systemic illness, audiometry, MRI brain
What menieres treatment is there?
vertigo attacks with prochlorperazine, lifestyle changes, trial of betahistine, vestibular rehab, hearing support, local steroid injections
Causes of vestibular neuritis/labyrinthitis?
usually from reactivation of latent herpes simplex, peak onset 40-50yrs; others = AI, microvascular ischaemic insults, URTI prior, viral, systemic disease
Labyrinthitis S+Ss?
when inflammation of membranous labyrinth and damage to vestibular and auditory organs, sudden and incapacitating vertigo, exacerbated by movement, hearing loss, N+V
Labyrinthitis complications?
cochlea trauma from vertebrobasilar ischaemia, meningitis, Meniere’s and aminoglycosides
Labyrinthitis differentials?
stroke, TIA, tumour
Labyrinthitis examinations?
CNs, ear, gait, mastoid tenderness, Weber’s, head-impulse, nystagmus
What causes conductive hearing loss?
wax, otosclerosis, otitis media, glue ear
What causes chronic sensorineural hearing loss?
environment noise, inherited, presbycusis (loss of acuity for high freq before 30)
What causes sudden sensorineural hearing loss?
ENT immediately; noise, gentamicin, mumps, acoustic neuroma, MS, vasculitis, stoke
What tests for sudden sensorineural hearing loss?
ESR, FBC, LFT, Panca, viral titres, TB, evoked response audiometry, CXR, MRI, lymph, nasopharyngeal culture
What can tinnitus cause?
Depression and insomnia
What causes tinnitus?
inner ear damage, hearing loss, wax, excess noise, injury, otitis media, post-stapedectomy, menieres, aspirin, loop diuretics, aminoglycosides
How to treat tinnitus?
exclude serious; psych support; tinnitus coping training; drugs don’t tend to help but can try hypnotics at night or misoprostol; masking with white noise/hearing aid; cochlear nerve section = drastic
What are the common causes of headaches?
non-organic pain syndromes, sinusitis (dull, constant ache over frontal and maxillary sinuses with post-nasal drip, worse bent over), migraine, meningitis, SAH, raised ICP, cranial arteritis, encephalitis (uncommon), venous sinus thrombosis (subacute with papillodema), tropical illness, intracranial hypotension
Examinations for headache?
fundoscopy, bp, temporal artery palpation, neuro exam, cognition
What can intracranial venous thromboses cause?
seizures, less common then arterial, death from trans tentorial herniation or oedema
Dural venous sinus S+Ss?
mainly sagittal or transverse; mainly headaches, vomiting, papilloedema, seizures, unusually cerebellar signs (sigmoid)
Cortical vein S+Ss?
stroke-like focal symptoms over days; seizures, sudden headaches
Types of tension headache?
episodic (<15 day per month) or chronic (usually meds)
Tension headache S+Ss?
pressure/tightness mild-moderate, N+V, gradual in onset and variable duration, responsive to OTC
Tension headache examination?
head, neck, fundoscopy, bp
Tension headache treatment?
ibuprofen first, amitriptyline for chronic
Migraine types?
either with aura and headache, without aura and headache or without headache and aura; first as child then improves as older, FH
Migraine S+Ss?
tired, irritable, depressed, difficulty conc, CHOCOLATE aggravating factors, headache last 4-72 hours, unilateral, pulsating, severe, N+V, photo/phonophobia, aura in 1 eye then spread, unilateral paraesthesia, allodynia, can have dysphasia/dysarthria, ataxia, hemiparesis, ophthalmoplegia
Migraine red flags?
papilloedema, new seizure, abnormal neuro, new onset cluster
Migraine diagnosis?
without aura cannot until 5 attacks, menstrual migraine after falling oestrogen, pulsing, worsens with exercise, unilateral
Migraine treatment and management?
address triggers, simple analgesic (aspirin/ibuprofen), prochlorperazine (N+V), diclofenac suppository if V, triptans (5HT1 receptor agonists), prophylaxis if 2+ per month and include beta blocker and amitriptyline, if not this then sodium valproate; acupuncture if treatments don’t work and sometimes cold/hot pack during attack; stop oral contraception as can worsen, should get ease of headache during pregnancy
Cluster headache risks/triggers?
head injury, smoking, alcohol, sleep disruption, heat, exercise, solvents; episodic = 2wks to 3months, chronic = 1 yr without remission
Cluster headache S+Ss?
bouts of 12 wks and at night, pain without aura rapidly over 10 mins, intense, penetrating, behind or around eye, forehead and temple, 45-90mins, restless, ipsilateral lacrimation, rhinorrhoea, nasal congestion
Cluster headache red flags?
change in headache pattern, new headache over 50, systemic illness, personality change, ICP high
Cluster headache treatment?
stop smoking, limit alcohol, good sleep, if acute then SC sumatriptan, O2; prophylaxis = verapamil (ECG monitor fortnightly) and if not then lithium
SAH causes?
usually from berry aneurysms in circle of Willis or arteriovenous malformations, mean age 50
RFs for SAH?
Ehlers-Danlos, Afro-Caribbean, marfans, neurofibromatosis, FH
SAH S+Ss?
thunderclap headache for few secs, vomiting, seizures, meningism 6 hours after, some with confusion, if after head injury then decreased consciousness and hemiparesis; prodrome of 3wks = headache, diplopia, dizziness, orbital pain
SAH examinations?
consciousness, ophthalmoscopy, neck stiffness, neuro, bp increase, if had seizure then AV malformation, CT in 24hours and angiography following, LP if CT negative but still suspect (xanthochromia), ECG, kernigs sign
SAH treatment and management?
reduce bleeding and complications, endovascular obliteration by coiling/clipping, intubation/ventilation/NG feed may be need, nitroprusside for hypertension, GCS check, keep hydrated to stop hyponatraemia
SAH complications?
cerebral ischaemia from vasospasm treated with nimodipine, hydrocephalus by ventricular drainage/LP, cognitive impairment
Other headaches?
primary stabbing (trigeminal neuralgia), primary cough, primary exertional (brough on by exercise 5mins-48hours), primary sexual (orgasm), primary thunderclap
Common causes of delirium?
hypoxia (COPD, pneumonia, pulmonary oedema, resp depression risk drugs, heart problems, anaemia, cyanide), metabolic disorders, drug abuse, iatrogenic, CNS (subdural, infections, postictal), infection, environment, delirium tremens (uncommon in alcohol withdrawal)
Head injury investigations?
GCS; haemodynamics; neuro; other injuries; CT head and cervical if <13 GCS, abnormal X-ray, cervical injury
Head injury treatment?
immobilise cervical spine (GCS<15, neck pain, focal neuro, paraesthesia), ABC, A+E (for: high energy injury, lose consciousness, amnesia, persistent headache, focal neuro signs, vomiting, seizures, visible trauma, suspected skull fx, >65, bleeding hx, anticoagulation, drug/alcohol, non-accidental injury)
Head injury neurosurgery?
decreasing GCS, progressive focal neuro, persistent coma, unexplained confusion >4hours, CSF leak
Head injury A+E management?
high dose mannitol, prophylactic AEDs, early nutritional support
Head injury complications?
raised ICP, amnesia, CSF leak, meningitis, intracranial haemorrhage, skull fx, diffuse axonal injury, seizures, concussions, cognitive impairment
What is an extradural haematoma?
blood between dura and bone
Causes of extradural haematoma?
fx of temporal/parietal bone damaging middle meningeal artery/vein; also in spinal column after LP/epidural
Extradural haematoma S+Ss?
headache, seizures, CSF otorrhoea/rhinorrhoea, decrease in GCS, facial nerve injury, limb weakness, visual field defects; Spinal – numbness, paraesthesia, altered reflexes, urinary incontinence
Extradural haematoma investigations?
XR skull/spine; CT (crescent shaped blood clot)
Extradural haematoma treatment?
maintain airway, trauma assess; ICP raised = osmotic diuretics; burr holes
Extradural haematoma complications?
neuro deficits, post traumatic seizures 1-3months
Subdural haematoma types and pathophysiology?
acute, subacute (3-7 days post), chronic (2-3wks after); tearing of bridging veins of venous sinuses/bleeding from damaged cortical artery
Subdural haematoma causes?
Blunt head trauma
Risks for getting a subdural haematoma?
elderly, kids, alcoholics
Subdural haematoma S+Ss?
shortly after moderate-severe injury, LOC, progressive if chronic, hx anorexia and N+V, neuro deficits (focal limb weakness, speech tricky, personality change)
Subdural haematoma investigations?
GCS, vital signs, neuro, external trauma, FBC, U+Es, LFTs, coagulation screen, CT head (lens shaped clot)
Subdural haematoma treatment and management?
severe = cervical spine immobilise, ABC, intubate, ventilate, mannitol if high ICP, treat coagulopathy, emergency craniotomy, clot evacuate
Subdural haematoma complications?
cerebral oedema, raised ICP, recurrent haematoma, seizures, permanent neuro deficit
Disordered cognition common causes?
acute confusional state (delirium – surgery, systemic infection, head injury, drugs, withdrawal, metabolic, hypoxia, stroke, nutritional [b12]), dementia
Disordered cognition S+Ss?
cognition impaired, perception, consciousness, memory, disorientated, sleep disorder, hallucinations, hyper/hypoactive
Disordered cognition uncommon?
AIDS, myxoedema, vasculitis, neoplastic, Huntington’s, hydrocephalus, vit deficiency, CJD
Dementia definition?
neurodegenerative with decline in many cognitive areas; diagnosis = hx, cognition testing, examine, rfs, med review
Dementia types?
AD, vascular (don’t use ach inhibitors/memantine), lewy body (cognitive, hallucinations, later parkinsonism, don’t use antipsychotics), fronto-temporal (behaviour change, disinhibited, emotional unconcern)
Dementia treatment?
memory clinic, no cognition affecting drugs, massage/music/aromatherapy, SSRI if depressed
Alzheimer’s S+Ss?
> 40yrs, global cognitive impairment, visuo-spatial loss, memory, verbal, executive planning, anosognosia (don’t understand things like plots of films), later is agnosia, behaviour change, irritable, psychosis
Alzheimer’s RFs?
environmental, genetic, other psych problems, beta amyloid peptide build-up plaques, loss of ache, downs
Alzheimer’s management and treatment?
ache inhibitors (donepezil, rivastigmine, galantamine but can exacerbate heart block and peptic ulcers), antigultamatergic (memantine), antipsychotics only for non-cognitive, specialist memory service and bp control
Causes of raised ICP?
mass lesions, neoplasms, abscess, focal oedema from infection/trauma, CSF circ disturbance, venous sinus obstruction, diffuse brain oedema, idiopathic intracranial hypertension
S+Ss raised ICP?
headache (red flags – nocturnal, early morning, coughing and moving head exacerbates), papilloedema, vomiting, lethargy, irritable, slow decision making, abnormal behaviour, pupillary changes, unilateral ptosis, hemiparesis, hypertension, slow irregular pulse
Raised ICP investigations?
CT/MRI head, glucose, renal function, electrolytes, osmolarity, monitor ICP in severe head injury, abnormal CT and GCS3-8
Raised ICP management and treatment?
maintain arterial O2 tension, normal vascular volume; treat = avoid pyrexia, manage seizures, CSF drain, head off bed, analgesic (morphine), sedate (IV propofol), neuromuscular blockade, mannitol, hyperventilate; depressive craniectomy is last line
What is hydrocephalus?
increase in CSF in ventricles; causes usually impaired absorption and increased secretion
Pathophysiology of hydrocephalus?
ventricular dilation; CSF permeates in periventricular white matter = damage; types = non-communicating/obstructive where CSF obstructed in ventricles, communicating = communication with ventricles and SA space from problem out of ventricles (thickening of leptomeninges, increase in CSF viscosity), ex vacuo = secondary to brain atrophy (Alzheimer’s), congenital = from no antenatal care, maternal hypertension, pre-eclampsia, foetal alcohol use; acquired = supratentorial masses, intraventricular haematoma, tumours
Hydrocephalus S+Ss?
infants = rapid head circ increase, increased limb tone; adults acute = headache, vomiting, papilloedema, impaired up gaze; gradual onset = cognitive deterioration, neck pain, N+V, double vision, incontinence
Hydrocephalus investigations?
CT (dilated lateral and 3rd plus abnormal 4th = posterior fossa mass, dilated lateral and 3rd + 4th normal = aqueduct stenosis)
Hydrocephalus treatment?
LP if communicating, no treatment if asymptomatic and stopped, shunt and external ventricular drain
What is normal pressure hydrocephalus?
ventricular dilation in absence of CSF change
S+Ss normal pressure hydrocephalus?
gait abnormal, urinary incontinence, dementia, pyramidal tract signs, brisk reflexes
Causes normal pressure hydrocephalus?
SAH, meningitis, idiopathic, head injury, CNS tumour
NPH investigations?
MRI/CT show ventricles, large volume LP shows normal CSF pressure, papilloedema none
NPH treatment?
acetazolamide (carbonic anhydrase inhibitor), repeated LP, ventriculoperitoneal shunt
Causes of dysphagia?
Alzheimer’s, brain tumours, ALS, GBS, HD, PD, CNS infections, stroke, trauma, polio, cerebral palsy, MS, muscular dystrophy; resp failure = ALS, MG, muscular dystrophy
Bulbar palsy S+Ss?
tremulous lips, weak/wasted/fasciculations tongue, drooling, absent palatal moving, dysphonia, articulation, neuro deficits in limbs (flaccid, weak, fasciculations)
Bulbar palsy causes?
diphtheria, polio, MND, syringobulbia, CVA, brainstem tumours, GBS
Pseudobulbar palsy definition?
disease of corticobulbar tracts, bilateral
Pseudobulbar palsy S+Ss?
paralysed tongue, absent palatal movements, dribbling, paralysed facial muscles, hyperreflexia of jaw, nasal regurg, emotionally labile, increased tone, reflexes and weak
Pseudobulbar palsy causes?
CVA, MND, MS, injury, high brainstem tumours, neurosyphilis
What is dysarthria and dysphasia?
• Speech disorder from muscle control (dysarthria), impairment of language (dysphasia)
Two types of dysphasia?
receptive dysphasia = difficulty comprehension, excessive dysphasia = difficulty in understanding
Causes of dysarthria?
UMN of cerebral hemisphere or LMN lesions of brainstem
Dysarthria S+Ss associated with causes?
slurred and weak voice is pseudobulbar palsy; slurred staccato from cerebellar lesions in MS; dysrhythmia, dysphonia, monotonous in PD; indistinct articulation, hypernasal, bilateral weakness in MND
Causes of dysphasia?
lesion of dominant hemisphere from CVA, dementia, injury
Dysphasia S+Ss associated with causes?
fluent but doesn’t make sense; excessive S+Ss = not fluent but understand how to construct; conduction = lesions of arcuate fasciculus, posterior parietal and temporal; deep = lesions of temporal lobe and word repetition problems
What is optic neuritis?
inflammation of optic nerve
Optic neuritis S+Ss?
triad = eye pain, reduced vision, reduced colour vision, others = light flashes, Uhthoff’s phenomenon, Pulfrich’s phenomenon, fatigue, low pupillary light reflex, papillitis; develops over hours/days and worse in heat
Optic neuritis investigations?
MRI, CXR for atypical (sarcoidosis), LP
Optic neuritis causes?
demyelinating ON
Optic neuritis management?
from demyelination and compensatory neuronal recruitment; use methylprednisolone or interferon beta
What is papilloedema?
optic disc swelling from high ICP
Papilloedema causes?
non-arteritic anterior ischaemic optic neuropathy, optic neuritis, intracranial patho (tumour, haemorrhage, trauma, infection, abscess, resp failue)
o If unilateral – ADON, retinal vein occlusion, diabetic papillopathy
o Bilateral – papilloedema, toxic optic neuropathy, malignant HT
Papilloedema S+Ss?
hours/wks, enlargement of blind spot, blurred vision and vision obscurations
Bell’s palsy S+Ss?
abrupt (usually after sleep) with complete unilateral facial weakness and ipsilateral ear ache; ageusia (low taste); can’t wrinkle forehead; sound hypersensitivity; others = unilateral mouth drooping, drooling, food trapped in gum + cheek, can’t close eye (red), ectropion, speech tricky, conjunctivitis
Differentials of Bell’s (if rash, bilateral, UMN signs, other CNs, limbs affected)?
infective (Lyme’s, meningitis), brainstem lesions, tumours, systemic disease (GBS, sarcoidosis)
Bell’s management?
Most completely recover; within 72hours prednisolone; protect eyes with glasses and artificial tears
What inheritance is type 1 and 2 neurofibromatosis?
AD
NF1 S+Ss?
café-au-lait spots, freckling in skin folds, dermal neurofibromas (can become papillomas), nodular fibromas, lisch nodules, mild LD, nerve root compressions, some get malignancy, GI bleeds and obstructions, cystic lesions, scoliosis
NF2 S+Ss?
more likely to get a bilateral vestibular schwannoma/malignancy; can get sensorineural hearing loss, tinnitus and vertigo
NF1 management?
MDT
NF2 management?
Brain MRI and treat malignancy
What is the syrinx?
tubular cavity close to or in cervical cord canal
What causes syringomyelia?
basilar invagination, masses, blocked CSF circ
Syringomyelia S+Ss?
absent pain and temp sensation; wasting/weakness of hand (claw); others = horner’s, UMN leg, body asymmetry; can get syringobulbia
Syringomyelia management and treatment?
MRI imaging; decompress at foramen magnum
S+Ss delirium?
cognitive (lower conc, slow response, confusion, disorientated in time), perception (hallucinations), physical (lower mobility and movement, restless, agitated, change in appetite, sleep disturbance; all with fluctuations), social (lack of cooperation, withdrawal, change in mood, delusional); hypo/hyperactive
Delirium management?
holistic; treat cause; avoid sedation if possible (antipsychotics first – haloperidol or olanzapine)
What is narcolepsy and patho?
• Narcolepsy – chronic neuro condition producing disruption to normal sleeping pattern; excessive sleepiness; starts around adolescence
o Thought to involve hypocretin (orexin)
o Triggers – head trauma, infection and change in sleep habits
o Usually have normal amount of sleep but is fragmented and a lot during the day; don’t have as much REM
Narcolepsy S+Ss?
o Presentation – triad of excessive daytime sleepiness (EDS), hypnagogic hallucinations and sleep paralysis
EDS – persistent sleepiness, nap during ADLs, excessive fatigue, automatism (episodes where seem awake but lack full awareness and behave inappropriately); autonomic (pupils abnormal, fainting spells, ED, night sweats, gastric problems, low body temp, systemic hypotension, dry mouth, heart palps, headache, extremities dysthermia); sleep paralysis = pts aware but can’t open/move eyes, sense of inability to breathe
Cataplexy definition?
sudden loss of muscle tone, preserved consciousness and power in response to strong emotion; only from narcolepsy (5%); last few seconds/minutes
Cataplexy S+Ss?
can be slight facial drooping to no muscles working aside from diaphragm; slurred speech, blurred vision, diplopia; hearing, awareness and consciousness intact; few times per day or less than 1 per year; usually bilateral weakness
Narcolepsy investigations?
Epworth sleepiness scale; sleep studies (nocturnal polysomnography); EEG; brain MRI to exclude lesions
Narcolepsy diagnosis?
excessive daytime sleepiness daily for 3months or more; cataplexy (may be there or not); not due to another condition; nocturnal polysomnography then MSLT
Narcolepsy differentials?
OSA, drug/toxins, seizures, syncope, TIA, sleep paralysis, psychosis
Narcolepsy management and medications?
good sleep hygiene, strategic daytime naps, reg exercise, family and friends educations, no known cure for cataplexy; stimulants for EDS, modanafil for EDS and may help with cataplexy, antidepressants (tricyclics) can improve sleep paralysis or hypnagogic hallucinations, benzos sometimes used
o EDS – first-line = modanafil, 2nd = methylphenidate, 3rd = modanafil with sodium oxybate
Narcolepsy complications?
poor conc, memory, falls/injuries in cataplexy, status cataplecitcus (if meds stopped abruptly), obesity, metabolic syndrome, impulsive
Shingles definition and S+Ss?
- Symptoms in dermatome; pain and rash (mild to severe; dull or stabbing); not usually widespread; usually chest, abdo and eye
- Rash 2-3 days after pain; red blotches and fluid filled blisters; can get scarring; lasts 2-4wks; sometimes fever; contagious through blisters until dry; only get shingles as a reactivation of own chickenpox (immunosuppressed/stress)
Shingles management and medications?
- Management – loose clothing; ice; emollients when itchy (calamine); dressing for blisters
- Pharma – NSAIDs, paracetamol, sometimes opiates if painful; if neuropathic pain then tricyclics or gabapentin; antivirals = acyclovir, famciclovir, valaciclovir (for over 50s, shingles in eye/ear, immunocompromised, moderate/severe pain, moderate/severe rash); steroids to reduce inflammation
Dopamine effect and receptors?
D1-5 receptors and mood and reward-seeking behaviour
Dopamine agonists and conditions for?
pramipexole/ropinirole/levodopa/apomorphine (parkinson’s), cabergoline (hyperprolactinaemia, acromegaly), chlorpromazine (schizophrenia), metoclopramide (nausea)
Serotonin effects and receptors?
5HT1-7 receptors and many effects
Serotonin agonists and conditions for?
lithium (mood stabiliser), sumatriptan (migraine), buspirone (anxiety), fluoxetine/sertraline (depression), ondansetron (nausea), mirtazapine (depression), olanzapine/clozapine (psychosis)
Types of amino acids and their effects?
glutamate and aspartate = excitatory on NMDA and non-NDMA in epilepsy and CNS ischaemia; GABA inhibitory
GABA agonists and their conditions for?
gabapentin/valproate (epilepsy and neuro pain), benzos (sedation), baclofen (spasticity), alcohol
Glutamate antagonist and what for?
memantine for dementia
Ach receptors?
muscarinic and nicotinic receptors
Peripheral agonists of ach?
glaucoma (pilocarpine), myasthenia gravis (anticholinesterases)
Peripheral antagonists of ach?
asthma (ipratropium), incontinence, dry secretions pre-op, dilate pupils, increase HR (atropine)
Ach inhibitors for dementia?
donepezil, galantamine, rivastigmine
Ach treatment for drug-induced parkinsonism?
procyclidine, trihexyphenidol
Types of histamine and purine treatments and what for?
cyclizine (antihistamine and nausea), purinergic receptor blocker (chronic pain)
Types of neuropeptides and what for?
exogenous opioids (wide range of analgesic and mood related effects); aprepitant (low chemo nausea)
Types of receptors for noradrenaline and adrenaline and their effects?
alpha and beta 1-2; alpha receptors = arteriolar vasoconstriction and pupillary dilation (peripheral); beta 1 = high pulse and myocardial contractility; beta 2 = bronchodilation, uterine relaxation, arteriolar vasodilation
What is clonidine for?
refractory hypertension
What are tricyclics and venlafexine for?
SNRIs and 5HT for depression
What is a TIA?
• No infarction; brief episode of neurological dysfunction from temporary focal cerebral ischaemia (loss of O2 to specific part of brain matter)
Pathophysiology of TIA?
small vessel occlusion (usually by atherothromboembolism from carotid but also cardioembolism giving microemboli and hyperviscosity of blood); usual risk factors for what would cause these (like for an MI)
S+Ss TIA?
sudden loss of function but then resolved after some minutes; most affect anterior circulation of brain (weak contralateral leg and sometimes arm; weakness on one side of body [hemiparesis]; dysphasia; amaurosis fugax [loss of vision in one eye] – think of what would happen in a stroke: FAST where face refers to eyes); posterior circ (diplopia, vertigo, vomiting, choking and dysarthria [not quite incoherent speech but difficult to understand], ataxia, hemianopia – think that posterior is more to do with how you would feel at top of high building – VERTIGO AND FEELING ILL AND STRUGGLING TO WALK PROPERLY)
Diagnosis of TIA?
based on description usually; bloods (look for anything that could lead to blood thickening); carotid artery doppler ultrasound for stenosis; all the scans (CT, ECG)
TIA treatment?
score risk of stroke after TIA (ABCD2 – SEE PAGE 38 – if score above 6 see specialist immediately); antiplatelets, anticoagulant for any other complications like AF etc, statins, control CV risk
Stroke definition?
Rapid onset (last more than 24 hours) neurological deficit by infarction
What is ABCD2?
A — Age: 60 years of age or more (1 point) B — BP (at presentation) 140/90 mm Hg or greater (1 point) C — Clinical features Unilateral weakness, 2 points Speech disturbance without weakness, 1 point. D — Duration (60 minutes or longer, 2 points, 10–59 minutes, 1 point) D — presence of diabetes: 1 point
Carotid ischaemic stroke S+Ss?
weakness of face, arm, legs; amaurosis fugax (painless loss of vision); impaired language
Posterior circ stroke S+Ss?
dysarthria, dysphagia, diplopia, dizziness, ataxia, diplegia
Anterior circ stroke S+Ss?
supplies frontal lobe bits so motor function affected and superior bits of parietal so a bit of integrating sensory information to give an output (leg weakness and sensory disturbance, apraxia, incontinence, drowsiness as consciousness from frontal lobe lost, decrease in spontaneous speech; MAINLY ONE SIDED)
Middle cerebral artery stroke S+Ss?
bits of frontal lobe again (mainly motor for head, neck and arms MAINLY FOR BOTH SIDES and this also incorporates speech areas – broca’s and wernicke’s) and a bit of parietal to do with visual for sight (hemianopia)
Posterior cerebral artery stroke S+Ss?
to do with supplying the occipital lobe (SEE END OF PAGE 43 FOR SPECIFICS OF BLINDNESS)
Vertebrobasilar artery stroke S+Ss?
supplies loads including cerebellum and pons linking cerebrum to cerebellum so can be v dangerous; motor, speech, visual and consciousness (basically all of the mentioned effects can be felt here)
Lacunar stroke S+Ss?
small strokes subcortically; deep penetrating arteries occluded; no cortical features; due to small vessel disease; pure motor hemiparesis, ataxic hemiparesis, clumsy hand and dystharthria, pure hemisensory, mixed sensorimotor
What does spinothalamic tract do?
lateral = pain and touch and medial = crude touch and on same side but cross before thalamus
What does spinocerebellar tract do?
proprioception (that’s input for cerebellum) and dorsal ipsilateral cerebellum and ventral contra and ipsilateral cerebellum
What does the spinoreticular tract do?
deep/chronic pain
What does the corticospinal tract do?
Control of voluntary muscles and pass to Cerebral peduncles (above this is pyramids [ventrolateral sulcus on lateral border of pyramid on either side continuous with spinal cord] to mark the corticospinal tract and can also see the decussation later in the midbrain like pyramids of Giza)
What does the tectospinal tract do?
head Turning for visual stimuli
What does the rubrospinal tract do?
spinal Reflexes
What does the vestibulospinal tract do?
like wearing a VEST for some at the gym who has big muscles for muscle tone and posture
What do the mammillary bodies do?
Make new Memories
What does the cerebellum do and what inhibits it?
excites motor control and Basal ganglia Blocks/inhibits it (thalamus)
What is a generalised tonic-clonic/grand mal seizure?
(think like how you would imagine a jerky seizure and stiff limbs like normal epilepsy) - no aura usually; lose consciousness; tonic phase = rigid limbs; clonic phase = some generalised muscle jerking for a couple of mins
What is a typical absence/petit mal seizure?
child; looks like child has zoned out for a couple of seconds and may not realise even had a seizure; can lead to tonic-clonic in later life
What is a myoclonic seizure?
sudden isolated jerk of part of the body and can throw them to the ground with an uncontrolled limb
What is a tonic seizure?
increase in muscle tone and stiffening (REMEMBER TONIC = STIFFENING)
What is an atonic seizure?
loss of muscle tone
What is a simple partial seizure?
no post-ictal symptoms and no impairment of awareness and memory and usually frontal lobe (THINK SIMPLE MEANS NO COMPLICATIONS AFTER)
What is a complex partial seizure?
affects awareness and memory (so usually temporal lobe therefore as affects speech understanding, memory and emotion as connected to the hippocampus etc); post-ictal confusion common
What is a partial seizure with secondary generalisation?
can start as partial but spread to general and cause convulsions
What hormone is raised after an epileptic rather than a non-epileptic attack?
Raised prolactin
Triad of normal pressure hydrocephalus S+S?
incontinence, confusion, dementia
