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A2 ME3031 NEURO > W11: Clinical Neurology & Neurosurgery > Flashcards

W11: Clinical Neurology & Neurosurgery Flashcards

1
Q

· Describe the clinical tests used to assess cranial nerve function

A

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

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2
Q

Describe tests of cranial nerve reflexes (interactive session)

A

pupillary: II + III
corneal: V + VII
jaw: V
gag: IX + X

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3
Q

State causes of eye movement disorders

A

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

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4
Q

Describe the clinical features of trigeminal neuralgia, Bell’s palsy and vestibular neuronitis

A

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

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5
Q

Describe the clinical features of pseudobulbar and bulbar palsy

A

LMN/UMN signs = speech and swallowing dysfunction

LMN

  • IX-XII
  • bilateral
  • MND, polio, tumours, syphillis
  • wasted fasciculating tongue

UMN

  • vascular
  • bilateral
  • dysphonia
  • spastic tongue
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6
Q

Describe the effects of the sympathetic and parasympathetic systems on pupillary responses and identify the causes of small and dilated pupils

A

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

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7
Q

Dementia syndromes: causes and diagnoses

A
  • 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

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8
Q

Dementia management

A

=> Non pharm support
=> Insomnia Tx
=> Antipsychotics: behaviour [caution: adverse in elderly]
=> Depression

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9
Q

Parkonsinism: causes and diagnoses

A

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)

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10
Q

Parksonism mgmt

A

=> 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
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11
Q

Consciousness & Coma

A

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

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12
Q

Testing for brain death

A

testing
pupillary, corneal, vestibular COWS, gagging reflexes
as well as pinching for pain and ventilator switched off momentarily

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13
Q

Define coma, consciousness and persistent vegetative state

A

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.

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14
Q

Locked-in Syndrome

A

Total paralysis apart from elevationdepression of eye + eye closure d/t paralysis below level of IIIn.

d/t PONTINE INFARCT (basilar art occ.)

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15
Q

GCS

A 
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
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16
Q

STROKE TYPES: LACS

A

1/4:

  • pure sens stroke
  • pure motor
  • sensori-motor stroke
  • ataxic hemiparesis

*recurrent in nature

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17
Q

STROKE TYPES: PACS

A

2/3:

  • unilateral weakness +/- sens deficit, face arm leg
  • homonymous hemianopia = inattention
  • higher cerebral dysfunction (dysphagia, visuospatial)
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18
Q

STROKE TYPES: TACS

A

3/3:

  • unilateral weakness +/- sens deficit, face arm leg
  • homonymous hemianopia = inattention
  • higher cerebral dysfunction (dysphagia, visuospatial)

*carotid artery or MCA

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19
Q

STROKE TYPES: POCS

A

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
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20
Q

Presentation of stroke

A

sudden onset of focal/global neurological deficits.

+ve symptoms = seizure, neuralgia, SAH

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21
Q

gaze palsy

A

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)

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22
Q

Cortical Blindness

A

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)

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23
Q

Mgmt of Stroke

A

=> 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)
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24
Q

Review arterial anatomy of the brain

A

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

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25
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
26
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.
27
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.)
28
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.)
29
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)
30
Indications and contraindication of performing a lumbar puncture
indications: nil 2º ↑ICP to lesion/tumour/obstruction therefore safe in communicating hydrocephalus
31
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
32
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
33
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
34
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 ```
35
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 ```
36
bitemporal hemianopia
chiasm
37
quadrantonopia
optic radiation / temporal lobe
38
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
39
Long tract signs
Associated with myelopathy - clonus: rapid contractions - upgoing plantars - hypertonic - Hoffman sign: flick middle finger - proprioception weakness
40
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
41
Cauda Equina syndrome
bilateral, pins+needles, bladder/bowel, saddle anaesthesia
42
Thoracic metastases
commoner than disc degen. = UMN in lower limb
43
List the common types of brain tumours
1º: - GB multiforme (neuroepithelial tissue) - meningioma - adenoma (pituitary) 2º: mets - renal cell carcinoma - lung - breast - melanoma - GI
44
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
45
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
46
Gerstmann's Syndrome
Dominant parietal lobe lesions = calculating, self-awareness sensory
47
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
48
Tx of GBmultiforme
=> complete sx excision => steroids + anticonvulsants => RT, CT
49
Commonest tumour types associated with cerebellum
Meningioma, arising from posterior cranial fossa
50
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
51
Munro-Kelly doctrine
Change in volume of contents or addition of new space occupying lesion increases pressure unless compensated by reduction of other content
52
↑ICP Pathology
-focal/global ↓blood flow=↓energy=pump failure = cell dysfunction = toxic metabolite = cell death -
53
pathophysiology of raised intracranial pressure and cushings reflex
``` ↑ICP = triad -HT - irregular breathing - bradycardia as a response from cerebral ischaemia OR brainstem distortion ```
54
Cerebral Perfusion Pressure
Difference between MAP and ICP
55
raised ICP results in a headache
prominent in morning d/t hypercapnic levels during the night s/t resp depression = vasodilation + ↓CSF abs.
56
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 -
57
management increased intracranial pressure
=> monitoring of ICP with surgically implanted pressure transducer => CPP monitoring and optimising CPP to prevent insult
58
Primary brain injury (focal and diffuse)
- Diffuse axonal injury - diffuse oedema -Herniation subtypes
59
Understand secondary brain injury and cushings reflex
following injury, progressive neuro deterioration ``` glutamate=calcium= oedema NO = vasodilation ```
60
Ischaemic injury
Wedge infarcts => areas more prone to damage, areas in between arterial supply
61
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
62
investgiation and management of TBI
=> CT, MRI => maintaining ICP and follow-up
63
intracranial aneurysms
aneurysm: thin wall vasc + hydroceph compl.; SUDDEN ONSET WORST HEADACHE CoW ∴ central lesion in imaging

A2 ME3031 NEURO (7 decks)

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