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
Define hydrocephalus
Abn accum of CSF in ventricles of brain
Non-communicating hydrocephalus: obstructive block in ventricular system.
Communicating: abn absorption @ arachnoid villi
*CSF overproduction d/t choroid plexus papilliomas.
classification of hydrocephalus
CONGENITAL:
CHIARI TYPE 2: spina bifida, hydrocephalus + neural tube defect
Aqueduct stenosis (2º consequence)
Dundy-Walker malformation: atresia of Leuschka & Magendie formation
ACQUIRED:
- infection; men. in childhood = communicating hydroceph (commonest)
- post-haemorrhagic = communicating hydroceph.
- 2º to masses (post. fossa tum.)
treatment of hydrocephalus
=> LP (communicating)
=> Lumbar drain
=> External ventricular drain in non-comm
=> Permanent diversion via endoscoping third ventriculostomy ETV (non-comm) or ventriculoperitoneal shunt - VP shunt (comm.)
Indications and contraindication of performing a lumbar puncture
indications: nil 2º ↑ICP to lesion/tumour/obstruction
therefore safe in communicating hydrocephalus
> potentially low ICP syndrome post (Rickets)
Indications and contraindication of performing a lumbar puncture
indications: nil 2º ↑ICP to lesion/tumour/obstruction
therefore safe in communicating hydrocephalus
Describe the necessary steps that must be taken in post lumbar puncture care, including management of any complications
potentially low ICP syndrome post (Rickets); headache
=> hydration
!coning
Symptoms of Hydroceph
↑ICP sign: papilledema (sensitive indirect), N/V, gait, upgaze/abducens palsy, morning headache
children: head circumference
*imaging: CT: mickey mouse
MRI
*USS: bone window in open fontanelles in babies
Be able to assess a patient who is obtunded, confused, or alert
OBTUNDED:
GCS - cerebral perfusion (CPP = MAP - ICP)
pupils - herniation & resulting compression of IIIn
CONFUSED: posture, neglect, mini-mental
ALERT: focussed neuro exam
Understand how to examine individual lobe of the brain
FRONTAL: posture + altered behaviour
- pyramidal weakness: pronator drift
- speech
- lack of motivation and executive funct.
OCCIPITAL: vision
CEREBELLUM: DANISH P dysdiadochokinesia ataxia nystagmus intention tremot slurred speech hypotonia past pointing
Understand how to examine individual lobe of the brain
FRONTAL: posture + altered behaviour
- pyramidal weakness: pronator drift
- speech
- lack of motivation and executive funct.
PARIETAL: body image, vis spatial, lang. numeracy
TEMPORAL: auditory input, lang., declarative LT mem., emotion, visual fields
OCCIPITAL: vision
CEREBELLUM: DANISH P dysdiadochokinesia ataxia nystagmus intention tremot slurred speech hypotonia past pointing
bitemporal hemianopia
chiasm
quadrantonopia
optic radiation / temporal lobe
Patterns in spine nerve pathology
Myelopathy: bilateral, motor+sens, UMN
Radiculopathy: unilateral, single myotome/dermatome pain/disturbance, ↓reflex, LMN
-prolapsed disc common
Peripheral nerve: unilat., m+s deficit in terriroty of nerve, LMN
Peripheral neuropathy: glove and stocking
Long tract signs
Associated with myelopathy
- clonus: rapid contractions
- upgoing plantars
- hypertonic
- Hoffman sign: flick middle finger
- proprioception weakness
L5 radiculopathy
common, pain along dorsum of foot. - ?altered sens - extensor hallucis longus weak? - pedal pulses: ?vascular pathology compression lower down spine
=> Neuropathic pain relief: AMITRYPTILLIN / GABAPENTIN
=> Discectomy
Cauda Equina syndrome
bilateral, pins+needles, bladder/bowel, saddle anaesthesia
Thoracic metastases
commoner than disc degen.
= UMN in lower limb
List the common types of brain tumours
1º:
- GB multiforme (neuroepithelial tissue)
- meningioma
- adenoma (pituitary)
2º: mets
- renal cell carcinoma
- lung
- breast
- melanoma
- GI
Primary brain tumours
GLIOMAS
derived from astrocytes, commonly grade IV, rare spread systemically
(frontal and temporal lobes commonest)
MENINGIOMAS
slow, benign, arise from arachnoid @ falx, convexity, sphenoid
PITUITARY: adenomas commonest
visual disturbance d/t optic chiasm + hormone imbalance
Discuss the ways in which patients with brain tumours present clinically, including signs and symptoms by tumour site
- ↑ICP = papilloedema, IIIn/VIn palsy
- focal deficit
- epileptic fits (tentorium lesions)
- CSF obstruction
Gerstmann’s Syndrome
Dominant parietal lobe lesions = calculating, self-awareness sensory
Brain tumour investigation & management
This is usually done with injection of an x-ray contrast (dye), though CT scan done even without the x-ray contrast is also sufficient as the first imaging test. MRI with injection of contrast is a more definitive and detailed imaging test which can detect or rule out a brain tumor in most cases.
Histology post Sx Tx.
=> Sx excision
=> Radiotherapy
=> Corticosteroids - swelling
Anticonvulsants, analgesia
Tx of GBmultiforme
=> complete sx excision
=> steroids + anticonvulsants
=> RT, CT
Commonest tumour types associated with cerebellum
Meningioma, arising from posterior cranial fossa
factors that cause a raised ICP and the body’s physiological response to such an insult
- straining, sneezing or getting up from recumbent position
- sustained 20cmH20+ = pathology
- significant impaired blood flow (hypoT, HT, hypoxia, ↑ICP) energy failure = cell death
Munro-Kelly doctrine
Change in volume of contents or addition of new space occupying lesion increases pressure unless compensated by reduction of other content
↑ICP Pathology
-focal/global ↓blood flow=↓energy=pump failure = cell dysfunction
= toxic metabolite = cell death
-
pathophysiology of raised intracranial pressure and cushings reflex
↑ICP = triad -HT - irregular breathing - bradycardia as a response from cerebral ischaemia OR brainstem distortion
Cerebral Perfusion Pressure
Difference between MAP and ICP
raised ICP results in a headache
prominent in morning d/t hypercapnic levels during the night s/t resp depression = vasodilation + ↓CSF abs.
Role of autoregulation
to maintain constant blood flow in-spite of wide variations in bp
- can ↑flow to specific regions when active
- ## Hypercapnia causes marked dilation of cerebral arteries and arterioles
management increased intracranial pressure
=> monitoring of ICP with surgically implanted pressure transducer
=> CPP monitoring and optimising CPP to prevent insult
Primary brain injury (focal and diffuse)
- Diffuse axonal injury
- diffuse oedema
-Herniation subtypes
Understand secondary brain injury and cushings reflex
following injury, progressive neuro deterioration
glutamate=calcium= oedema NO = vasodilation
Ischaemic injury
Wedge infarcts => areas more prone to damage, areas in between arterial supply
State the different types and clinical features of head injury: Extradural, subdrual, subarachnoid haemorrhage
Diastatic fracture: suture lines, children
Contusions: bruising; coup + contrecoup
EDH: direct impact, egg/lens haemotoma/hours; peeling dura off skull, lucid interval prior to deterioration
SDH: bridging veins; crescent; beneath dura; elderly d/t atrophy, anticoag use, falls. rarely from other causes
- longer presentation nature
- chronic w/ elderly: re-bleeding/expansion exerting pressure. low ICP patients.
SAH: aneurysm or trauma.
+ventricle involvement.
• aneurysm: thin wall vasc + hydroceph compl.; SUDDEN ONSET WORST HEADACHE
• peripheral haem. with traumatic VS central aneurysm.
-hypertensive intracranial haemorrhage/stroke = intracerebral haemorrhages
DAI: trauma/shearing (RTA); hypoxia; ischaemia; hypoglycaemia
- unconcious since onset.
FAT EMBOLISM: trauma+longbone fracture (BM emboli) = lodging in lung and cranial vasc.
- dyspnea, hypoxia, confusion
investgiation and management of TBI
=> CT, MRI
=> maintaining ICP and follow-up
intracranial aneurysms
aneurysm: thin wall vasc + hydroceph compl.; SUDDEN ONSET WORST HEADACHE
CoW ∴ central lesion in imaging
