W11: Clinical Neurology & Neurosurgery Flashcards
· Describe the clinical tests used to assess cranial nerve function
CN V: cornea test
+mastication
+ jaw jerk
CN VII: facial expr. + corneal reflex
CN VIII: rinne - bone conduction weber - conduction & sesorineural Dix-halpike: vestibular function Unteberger's: marching eyes closed
CN IX + X: palate movement, gag reflex, speech quality
CN XI: SCM+traps symmetry and strength
- shrug
CN XII: tongue: appearance; power; movement
Describe tests of cranial nerve reflexes (interactive session)
pupillary: II + III
corneal: V + VII
jaw: V
gag: IX + X
State causes of eye movement disorders
CN III PALSY - affected side = corresponding eye down+out @ neutral and inability to adduct
CN IV PALSY - affected side = eye turns upwards, hyperelevation as it moves medially
CN VI - affected side = eye turns inwards @ neutral (LR absence), inability to abduct
Describe the clinical features of trigeminal neuralgia, Bell’s palsy and vestibular neuronitis
trigeminal neuralgia: unilateral / mandibular maxillary stabbing sensation (d/t phys. env. trigger) d/t vascular compression of nerve root
BELL’S PALSY: CN VII = face weakness, pre-auricular pain. !eye care
=> steroids
VESTIBULAR NEURONITIS: disabling vertigo, sudden onset ?viral cause
Describe the clinical features of pseudobulbar and bulbar palsy
LMN/UMN signs = speech and swallowing dysfunction
LMN
- IX-XII
- bilateral
- MND, polio, tumours, syphillis
- wasted fasciculating tongue
UMN
- vascular
- bilateral
- dysphonia
- spastic tongue
Describe the effects of the sympathetic and parasympathetic systems on pupillary responses and identify the causes of small and dilated pupils
Pupillary responses:
parasympatethic innervation produces
= MIOSIS (CN II and III) via circular muscle contraction
via the Edinger-Westphal Nucleus of the IIIn
sympathetic innervation produces
= MYDRIASIS of pupil via radial muscles contracting
via the superior cervical ganglion
Dementia syndromes: causes and diagnoses
- CSF (inflamm), CT/MRI, EEG, Mini Mental exam, Neuropsychological assessment
!infective, deficient, and endocrine causes + mimics!
ALZHEIMER’S DISEASE: APOE; APP; PSEN1 + 2, SMOKING OBESITY DM, HT
- B AMYLOID PLAQUES AND NF TANGLES
- commonest
DEMENTIA w/ LEWY BODIES α-synuclein = early vis spatial + executive symptoms \+ prominent fluctuation * Parkinsonism + vis. hallucination => Cholinesterase inhibitors => Donepezil => NMDA antagonist
FRONTOTEMPORAL DEMENTIA
Tau pathology = early personality loss + eating habit and hbehavioural; dysphagia
*memory+spatiovisual reserved
*young onset
TEMPOROPARIETAL DEMENTIA
early memory loss + lang, visspatial loss
*personality preserved
VASCULAR DEMENTIA
mixed picture + STEPWISE decline
* young onset
Dementia management
=> Non pharm support
=> Insomnia Tx
=> Antipsychotics: behaviour [caution: adverse in elderly]
=> Depression
Parkonsinism: causes and diagnoses
RF: LRRK2 (AutoDom.) late onset; Parkin (recessive) young onset, GBA, pesticide, M > F
dopamine loss + lewy bodies in BASAL GANGLIA
IDIOPATHIC: dementia w/ Lewy
DRUG INDUCED: dopamine antagonist
VASCULAR PARKINSONISM: lower half of body
PARKINSONS + : multi system atrophy, progressive supranuclear palsy + corticobasal degen.
- bradykinesia
- rigiditiy
- tremor
- postural instability
[ asymm. resting tremor ] responsive to dopamine replacement Rx - expressionless face + progressive detriment
pre-onset: anosmia, REM disorder, urinary/bowel, neuropsychiatric
- dopamine transporter SPECT (imging)
Parksonism mgmt
=> LEVODOPA (dopamine precursor)
=> DOPA DECARBOX ENZYME INHIB.: CARBIDOPA; BESERAZIDE
=> COMT inhibitor: TALCAPONE
prevents dopamine breakdown
=> ROPINIROLE: dopamine agonist @ post-synaps.
!psychiatric complications
!levodopa wears off = motor fluctuations
Dyskinesias
LT: => MAO-B inhib. SELEGILINE: ↑1/2L of levodopa by preventing breakdown => Oral agonists => Continuous infusion => Deep brain stimulation => MDT and care package
Consciousness & Coma
ascending reitcular activating system => arousal
cerebral cortex => awareness
↓GCS d/t
- toxic/metab
- seizures
- dmg to ascending reticular activating system (stroke)
- TICP: tum.; stroke; EDH etc.; hydrocephalus
-Metabolic encephalopath d/t intoxication most common
Testing for brain death
testing
pupillary, corneal, vestibular COWS, gagging reflexes
as well as pinching for pain and ventilator switched off momentarily
Define coma, consciousness and persistent vegetative state
COMA: UNROUSABLE PSYCHOLOGICAL UNRESPONSIVENESS nil response to external stimulus
VEGETATIVE STATE: person appears to be awake but does not respond meaningfully to the outside world.
Locked-in Syndrome
Total paralysis apart from elevationdepression of eye + eye closure d/t paralysis below level of IIIn.
d/t PONTINE INFARCT (basilar art occ.)
GCS
EYE nil +1 pain +2 speech +3 spontaneous +4
VERBAL nil +1 incompr. +2 inappt. +3 confused +4 orientated +5
MOTOR nil +1 extens pain +2 flex pain +3 withdraw +4 to causing pain +5 command +6
STROKE TYPES: LACS
1/4:
- pure sens stroke
- pure motor
- sensori-motor stroke
- ataxic hemiparesis
*recurrent in nature
STROKE TYPES: PACS
2/3:
- unilateral weakness +/- sens deficit, face arm leg
- homonymous hemianopia = inattention
- higher cerebral dysfunction (dysphagia, visuospatial)
STROKE TYPES: TACS
3/3:
- unilateral weakness +/- sens deficit, face arm leg
- homonymous hemianopia = inattention
- higher cerebral dysfunction (dysphagia, visuospatial)
*carotid artery or MCA
STROKE TYPES: POCS
One of the following:
- CN palsy + contralateral deficit
- Bilateral deficit
- Conjugate eye movement disorder (gaze palsy)
- Cerebellar dysfunction (ataxia, nystagmus, vertigo)
- Isolated homonymous hemianopia / cortical blindness
Presentation of stroke
sudden onset of focal/global neurological deficits.
+ve symptoms = seizure, neuralgia, SAH
gaze palsy
The most common cause of vertical gaze palsy is damage to the top part of the brain stem (midbrain), usually by a stroke or tumor. In upward vertical gaze palsies, the pupils may be dilated. When people with this palsy look up, they have nystagmus. That is, their eye rapidly moves upward, then slowly drifts downward.
(POCS)
Cortical Blindness
Cortical blindness (CB) is defined as loss of vision without any ophthalmological causes and with normal pupillary light reflexes due to bilateral lesions of the striate cortex in the occipital lobes
(POCS)
Mgmt of Stroke
=> Thrombectomy
=> TPA (thrombolysis) + Thrombectomy (time sensitive <4.5hr onset)
=> Stroke unit
=> Aspirin
2º Prevention: antiHT, antiPl. Lipid lowering Warfarin (AF) =>Carotid endartectomy (ICA stenosis - symptomatic)
Review arterial anatomy of the brain
ACA + AComCA
ICA: gives off opthalmic artery and MCA
PComCA
PCA
superior cerebellar artery
BASILAR ARTERY + Pontine arteries
Anterior inferior cerebellar artery: gives off labyrinthine ar.
VERTEBRAL ARTERIES + Posterior inferior cerebellar artery
CSF
shock absorber for CNS, immunological akin to lymphatics.
produced choroid plexus (lateral ventricle) > abs in arachnoid granulations @ dural venous sinuses
clear. fluid, nil cells, (5-20cmH20), 2.5-3.5mmol/L of glucose
bacterial: PMN
viral + fungi: monocytes