Deck 11 Flashcards
Acute neuro lesions
Could be vascular, episodic or infective
Subacute neuro lesions
could be inflammatory, neoplastic or infective
Chronic neuro lesions
could be degenerative, neoplastic or infective
movement based neuro lesions
consider basal ganglia, cerebellum (ipsilateral) or corticospinal
sensation based neuro lesions
could be dorsal column (crosses after nuclei in medulla) or spinothalamic (cord cross)
Cord lesions
Generally bilateral unless brown sequard syndrome
Brainstem lesions
ipsilateral CN sign, contralateral peripheral nerve sign
Brainstem infarction often has vertigo as finding
nerve root pattern
pain at nerve root, then on corresponding dermatome
focal nerve lesion
isolated lesions (although if multiple then mononeuritis multiplex) Could be diabetes or vasculitis
Peripheral neuropathy
Sensory defect, may have weakness. Typically distal, symmetrical, glove and stocking. Typical of diabetes
muscle disease features
weakness only, no sensory issues
Myasthaenia gravis
arms, legs, eyes and mouth
Progressive weakness over the course of the day. NMJ pathology
Problem at right optic nerve
monocular vision loss (R)
optic chiasm lesion
Bitemporal heminaopia)
If pituitary tumour, may get superior quadrantanopia
If craniopharyngioma, carotid aneurysm or meningioma then may get inferior quadrantanopia
Right optic tract lesion
honomymous hemianopia (left visual field defect)
Problem at right temporal lobe (optic lesion)
Meyers loop - superior quadrantanpia of left visual field
Problem at right parietal lobe (optic lesion)
causes inferior quadrantic heminaopia of left visual field
Problem at cortex (e.g. right) - optic lesion
contralateral (left) homonoymous hemianopia (macula sparing)
CNIII lesion
ptosis, mydriasis, down and out eye (unopposed SO)
CNIV lesion
nasal upshot, vertical diplopia. Head tilts away from affected side
CNVI lesion
abduction issue, slight adduction in forward gaze
CNVII lesion
See frontal sparing in UMN lesion, or complete paralysis in Bell’s or ramsay hunt
CNX lesion
uvula deviates away from affected side, soft palate fails to rise
CNXII
tongue deviates towards affected side
Investigation with sudden neurological deficit
Urgent CT
Distinction between stroke and TIA
stroke is sudden onset syndrome of neurological distubance lasting 24h plus or leading to death. TIA reverses within 24h.
TIA can include amaurosis fugax lasting 1 min to 1 hour.
amaurosis fugax
seen in TIA, papiloedema (seconds), migrane aura (up to 30 mins)
Thalamus blood supply
Supplied by posterior cerebral artery - ischaemia causes sensory loss/distubance)
Brainstem blood supply
Basilar, superior cerebellar, anterior inferior cerebellar. Ischaemia gives limb weakness, sensory loss, CN palsy, locked in syndrome
Cerebellum blood supply1
Superior, anterior inferior and posterior inferior cerebral arteries. Ischaemia causes vertigo, ataxia, nystagmus and cerebellar signs
Occipital lobe blood supply
Posterior cerebral artery, ischaemia causes visual field defect
Ischaemic stroke on CT
dense artery
Stroke types
85% ischaemic (can be thrombotic, embolic, systemic hypoperfusion, vasculitis (systemic inflammation promotes pro-coagulation state). 15% haemorrhagic
Stroke RF
HTN, T2DM, hyperlipidaemia, AF, smoking, carotidy artery disease, obesity, metabolic syndrome, age, menopaiuse, male FHx, non white, syphillis
Lacunar infarctions
microinfarcts, arteriolosclerosis - often affects basal ganglia.
Can give vascular dementia
global ischaemia
Infarcts at boundary zones (watershed infarction) - if severe can give vegetative state (post arrest syndrome)
ischaemia parts (e.g. penumbra)
infarct core, oligaemic periphery (needs collateral supply) and ischaemic penumbra in betweeen (variable outcome tissue)
Stroke histology
1-2 days: axon hypoxia, myelin unravels, axons swell and degenerate (softening)
1-2 weeks, core disintegrates, neovascularisation and digestion of products
1-2 months -astrocytes proliferate and cause a glial scar around infarct
TACS
From internal carotid, affects anterior and middle cerebral arteries.
Causes hemivisual defect (MCA) - honomymous hemianopia), weakness/sensory defecit and higher cortical dysfunction (loc, dysphasia, visuospatial awareness)
PACs
As per TACS , but only 2 of
○ Hemivisual defect from optic radiation dysfunction via MCA (homonomyous hemipanopia)
○ Weakness/sensory deficit
Higher cortical dysfunction (LoC, dysphasia, visuospatial awareness)
POCS
1 of:
○ CN palsy and contralateral motor/sensory deficit
○ Bilateral motor/sensory deficit
○ Conjugate eye movement disorder
○ Cerebellar dysfunction (ataxia, nystagmus, vertigo)
Isolated honomymous heminapia or cortical blindness
Haemorrhagic stroke causes
HTN, trauma, bleeding disorder, amyloid angiopathy, cocaine, amphetamines, vascular malformations, bleeding into tumours, aneurysmal rupture and vasculitis.
Investigation of stroke risk
- Carotid doppler for atherosclerosis (size of plaques, degree of stenosis)
Echocardiogram/24h holter (AF, mitral valve disease, cardiac thrombus or valve vegetations
Stroke complications
Cognitive impairment, MI, HF (through autonomic dysfunction), dysphagia, aspiration pneumonia, UTI, DVT, PE, dehydration, malnutrition, pressure sores, depression, ortopoedic complications/contractures
Large cerebral infarcts can cause death by associated tissue oedema and herniation (malignant MCA syndrome).
Thunderclap headache
Acute, builds to max intensity within 5 minutes
Can indicate IC haemorrhage, venous sinus thrombosis, hypertensive encephalopathy, vertebral artery dissection
RF for subarachnoid haemorrhage
HTN, PCKD, ehler danlos, NF1, Marfan’s, alcoholism, smoking, clotting abnormality
1.6x more common in women
2x more common in black people
Presentation of subarachnoid haemorrhage
Severe headache
May have brief Loc, N&V, meningismus (aseptic meningitis)
May have seizures
Elderly people may present as seizure, confusion and mild headache/focal neurology
Mechanism of subarachnoid haemorrhage
normally aneurysmal, but can be AV malformation or cryptogenic, or can be trauma
Complications from subarachnoid haemorrhage
rebleed, seizure, vasospasm, hydrocephalus, electrolyte abnormalities, ECG abnormalities (ST depression, T wave inversion -may mimic MI), pulmonary oedema
Initial investigation for subarachnoid haemorrhage
CT within 6h (not as good after this)
LP if 12h since presentation (CSF xanthochromic on visual inspection)
CT/MRI angiography if fit for surgery
Most common cause of painful CNIII palsy
PCA aneurysm
acute subdural haemorrhage
Symptoms (Loc, low GCS, anisocoria, motor deficit) with 72h
On May have lucid interval,
CT shows hyperdense (white) blood
Needs surgical evacuation
subacute SDH
occurs over 3-7 days
Chronic SDH
over 2 weeks. May have subtle signs.
Blood on CT may be dark as older.
May be managed surgicall or conservatively
RF for SDH
Age (cerebral atrophy and increased venous fragility), alcohol, seizures, anticoagulants, bleeding disorders, head trauma, IC surgery.
Complications from SDH
Death due to cerebellar herniation, raised ICP, cerebral oedema, recurrent haematoma formation during recovery, seizures, wound infection, subdural empyema, meningitis, permanent neurological/cognitive deficit, coma/vegetative state
Meningism
Triad of photophobia, headache and nause
Signs of meningism
Brudinski sign, kernig’s sign, nuchal nigidity
Brudinski sign
flex neck causes hip flex
Kernig’s sign
knee extension elicits pain/resistance
Nuchal regidity
resistance to passive neck flexions
Meningitis
inflammation of leptomeninges, can be acute, subacute or chronic
Can be infective or not
Can be pyogenic or aseptic
Infective meningitis
In infectious causes, get localised infection in host, haematogenous seeding and either direct contiguous spread, or retrograde neuronal pathways allowing CNS entry.
Meningitis S+S
Typically headache, fever and neck stiffness
Also photophobia, N&V, URTI prodrome, seizures, focal neurological symptoms, lethargy, coma, stupor
Signs include pyrexia, non blanching petechiae (meningococcaemia), morbiliform rash with phatyngitis and adenopathy and vesicles (viral), endotoxic shock, Arthritis (N. meningitidis), extracranial infection (sinusitis, otitis media, mastoiditis, pneumonia)
Meningitis associated neurological signs
- Impaired consciousness
- CN palsy (esp 3, 4,6 or 7 - can be through direct damage or from raised ICP)
- Papilloedema
- Focal/generalised seizures
- Focal neurological signs (hemiparesis, dysphasia, hemianopia)
Sensorineural deafness)
Common bacterial meningitis pathogen
Streptococcus pneumoniae, neisseria meningitidis (H influenzae and listeria are more in I/compromise, pregnancy, age extremes)
common viral meningitis pathogens
(enterovirus, HSV, VZV, EBV, mumps, coxsackie)
Neisseria meningitidis classical presentation
petechial rash, occurs in small epidermics
Common themes for streptococcus pneumoniae meningitis
skull fracture, ear disease or congenital CNS lesions
Investigations for meningitis
- ABCDE
- Bedside tests (FBC, U&E, LFT, CRP, clotting, blood culture, meningococcal/pneumococcal PCR, lactate, glucose, throat swab (1x virology, 1 x bacteriology). May do stool sample or HIV test? May do throat swap?)
- Imaging (CT as quick)
LP (unless signs of raised ICP (focal neurological signs, GCS<12, seizures or papilloedema). Must record opening pressure if patient can lie down to get it (falsely high if patient is sitting up)- perform protein content, cell count, MC+S, glucose (plus serum glucose), vPCR (24-48h)
CI LP in meningitis
Raised ICP (papilloedema, focal neurological signs, GCS<12,), signs of meningococcal septicaemia, evidence of bleeding risk (platelets <50, INR>1.2), Hx of clotting disorder, rash/infection at LP site
Raised LP pressure in meningitis
Bacterial meningitis
May also be raised in fungal/TB
Normal LP pressure in meningitis
Viral (sometimes, fungal/TB)
WCC raised in LP for meningitis
Bacterial, viral
Mvariable in fungal/TB
polymorphs in CSF for meningitis
Bacterial
Lymphocytes in CSF for meningitis
viral, fungal, TB
protein increase in CSF for meningitis
bacterial (small rise in viral, fungal and TB)
Glucose reduced in CSF for meningitis
Bacterial (slight decrease in fungal/TB) - normal in viral
Turbid CSF in meningitis
bacterial
Viscous CSF in meningitis
viral
gram positive intracellular diplococci in CSF for meningitis
pneumococcus
Gram negative cocci in CSF for meningitis
meningococcus
ID TB or fungi in CSF
Ziel neelson stain for acid fast TB, indian ink for fungi
Management of bacterial meningitis
Tx with Abx immediately. Use steroids, notify public health
Viral meningitis Tx
Main symptoms are fever, seizures and change in mental state. Benzo’s useful for seizures, Aciclovir for virus.
CT may be normal in viral encephalitis, MRI often shows changes
Cerebral abscesses
headache, fever, altered mental status, focal signs/seizures. Often spread from sinus or blood. CSF may not show much so imaging is key
Immunocompromise patients with meningitis
HIV+, chemotherapy, alcoholism. Can be atypical organisms e.g. toxoplasmosis, cryptococcus, TB, aspergillus)- may not respond to ceftrioxone.
Acute complications in bacterial meningitis
sepsis, DIC, hydrocephalus, adrenal haemorrhage (waterhouse friderichsen syndrome)
Long term complications in bacterial meningitis
brain abscess, seizure disorder, CN palsy, sensorineural hearing loss, atazia Brain abscess (rare
peripheral causes of unilateral facial weakness
Ischaemia, bell’s palsy, sarcoidosis, GB syndrome, Lyme disease, otitis media, Ramsay Hunt Syndrome, cholesteatoma, parotid tumour
Cholesteatoma
keratinising squamous epithelium within the middle ear or in pneumatised areas of temporal bone. The growth expands, promoting bone reabsorption. Patient presents with hearing loss/ tinnitus, chronic/recurrent aural discharge (unresponsive to Abx) - discharge is generally malodorous. Patient may present with otalgia, vertigo, CNVII involvement (weakness or altered taste). Otoscopy typically shows crust in attic space (upper part of middle ear).Most commonly caused by repeated otitis media, but can be congenital (typically see white mass behind intact tympanic membrane) - congenital form is associated with cleft palate, craniofacial abnormality and chromosomal disorders.
Sarcoidosis affecting facial muscle
chronic granulomatous disorder, unknown aetiology, affecting lungs, skin and eyes but also other organs. Forms non-ceseating granulomas. Generally classed by organ involvement (ststemic, pulmonary, cutaneous, ocular, cardiac, neuro)- neuro causes headaches and seizures.
Lyme disease affecting facial muscle
- Lyme disease starts with erythema migrans 1-2weeks. Has constitutional symptoms (flu like prodrome). Often affects CNVII nerve.
Bell’s palsy
idiopahic. CNVII inflammation at geniculate ganglion, may be due to HSV-1. Causes LMN pathology. No neurological features. Management is by antivirals, steroids and eye care.
Ramsay hunt syndrome
- Ramsay hunt is caused by herpes zoster. Reactivates with geniculate ganglion on facial nerve, but can spread to CNVIII, CNV, CNIX and CNX. Causes ipsilateral facial paralysis, ear pain and vesicular rash. Management is with antiviral, oral steroids and analgesia. Prognosis is less good compaired to bell’s palsy
myaesthenia gravis
Autoantibodies bind to AcH at NMH. Muscles fatigue on exercise. Often associated with other autoimmunes. Diagnosed by Ach autoantibodies. Can have myasthenic crisis where respiratory failure occurs due to respiratory muscle weakness. Needs intubation and ventilation. Management uses acetylcholinesterase inhibition and immunosuppression
CNS causes of unilateral facial weakness
stroke, brain tumour (primary or metastatic), MS
Facial nerve pathway
Arises in pons
Travels through IAM
Enters facial canal
Sensory and motor roots fuse (facial nerve proper) and geniculate ganglion forms
Gives off: Greater petrosal (parasympathetic to mucous and lacrimal glands), nerve to stapedius (motor fibres to stapedius in middle ear), Chorda tympani (taste to anterior 2/3 of tongue), parasympathetic fibres to submandibular and sublingual glands
Also has extracranial branch (posterior auricular nerve for muscles around ear) and motor to digastric and stylohyoid
Motor branches of CNVII
Temporal zygomatic, buccal, marginal mandibular cervical
Anterior cerebral artery serves
medial surface of cerebral hemisphere
middle cerebral artery serservesves
2/3s of lateral surface of brain, central branches supply corpus striatum, thalamus and internal capsule
PCA serves
Corps callosum, occipital/temporal lobes, central branches supply optic radiation, subthalamic nucleus and thalamus
CNIII functions
somatic to 4/6 extra ocular muscles, levator palpebrae superioris. Visceral motor to pupil constriction.
CNIX functoins
gives stomatic to stylopharyngeus (swallowing assistance), visceral motor to parotid, special sensory to posterior 1/3 of tongue, general sensation to external ear and pharynx and visceral sensory from carotid body
CNX functions
gives somatic motor to palatal/laryngeal/pharyngeal swallowing muscles; visceral motor to trachea, bronchi, GI and heart smooth muscle; visceral sensory from same viscera; special sensory from epiglottis/palate, general sensory from auricle and EAM
CNI nuclei
olfactory epithelium
CNII nuclei
retinal ganglion
CNIII and CNIV nuclei
midbrain
CNV, CNVI and CNVII nuclei
pons
CNVIII nuclei
vestibular/spiral ganglion
CNIX, CNX and CNXII nuclei
medulla
CNXI nuclei
spinal cord
Bulbar palsies
Medullary, so CNIX, CNX and CNXII LMN lesions
Flaccid, wasted, fasciculating tongue
Dysphagia
Poor uvula elevationQuiet nasal speech
Jaw jer/gag reflex
Common causes for bulbar palsy
MND (degenerative), brainstem stroke (vascular), GB (inflammatory ), botulism (infective, neoplastic or congenital
Pseudobulbar palsy
Bilateral UMN lesion of medullary cranial nerves (so mimics LMN lesion).
Can get exagerated jaw jerk, mood disturbance, spastic tongue
Most common causes are MDN (degenerative), vascular (stroke), MS and head trauma
MND presentation for bulbar/pseudobulbar palsy
Often mixed presentation, fasciculating tongue with brish jaw jerk
Frontal cerebral lesion
ntellectual impairment, personality change, urinary incontinence, hemiparesis and Broca’s aphasia (if left frontal)
Left temporo-parietal lesions
agraphia, alexia, acalculia, Wernicke’s aphasia, contralateral sensory neglect
Right temporo-parietal lesions
face blindness, cotralateral sensory neglect
Cerebellar lesion stmptoms
- Broad ataxic gate (assess with heel-toe walk and Romberg’s test for sensory ataxia)
- Titubation (rhythmic head tremor)
- Dysarthria (slurred, staccato speech - Baby hippopotamus/british constitution
- Nystagmus
- Dysmetric saccades
- Upward drift (as per pronator drift but arms move up)
- Rebound phenomenon (eyes closed, arms raised, push arm down as patient resists - arm shoots up)
- Hypotonia (decreased in pure cerebellar disease)
- Mild hyporeflexia
- Dysmetria (finger to nose)
Dysdiadochokinesis
Causes of cerebellar dysfunction
alcohol, drugs (phenytoin), paraneoplastic cerebellar degeneration (seen in breast cancer and small cell lung cancer), severe hypothyroidism
Unilateral defect in MS, stroke, tumours (acoustic neuroma, meningoma)
Basal ganglia lesions
- Braadykinesia
- Muscle rigidity
- Tremor
- Athetosis (writhing of face/hands/tongue)
- Chorea
Hemiballismus (violent involuntary movements, proximal muscles of 1 arm)
UMN lesion causes
VINDIE (vascular - stroke, inflammatory - MS/MSN, neoplastic, Degenerative - parkinson’s, Infective - post meningitis, extra (drugs)
LMN lesion causes
NMJ (MG), peripheral nerve pathology, ventral horn pathology (MND/post polio), muscular pathology
