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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe tests of cranial nerve reflexes (interactive session)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dementia management

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

STROKE TYPES: LACS

A

1/4:

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

*recurrent in nature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

STROKE TYPES: PACS

A

2/3:

  • unilateral weakness +/- sens deficit, face arm leg
  • homonymous hemianopia = inattention
  • higher cerebral dysfunction (dysphagia, visuospatial)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Presentation of stroke

A

sudden onset of focal/global neurological deficits.

+ve symptoms = seizure, neuralgia, SAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CSF

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Define hydrocephalus

A

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
Q

classification of hydrocephalus

A

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
Q

treatment of hydrocephalus

A

=> 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
Q

Indications and contraindication of performing a lumbar puncture

A

indications: nil 2º ↑ICP to lesion/tumour/obstruction

therefore safe in communicating hydrocephalus

> potentially low ICP syndrome post (Rickets)

30
Q

Indications and contraindication of performing a lumbar puncture

A

indications: nil 2º ↑ICP to lesion/tumour/obstruction

therefore safe in communicating hydrocephalus

31
Q

Describe the necessary steps that must be taken in post lumbar puncture care, including management of any complications

A

potentially low ICP syndrome post (Rickets); headache

=> hydration

!coning

32
Q

Symptoms of Hydroceph

A

↑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
Q

Be able to assess a patient who is obtunded, confused, or alert

A

OBTUNDED:
GCS - cerebral perfusion (CPP = MAP - ICP)
pupils - herniation & resulting compression of IIIn

CONFUSED: posture, neglect, mini-mental

ALERT: focussed neuro exam

34
Q

Understand how to examine individual lobe of the brain

A

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
35
Q

Understand how to examine individual lobe of the brain

A

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
Q

bitemporal hemianopia

A

chiasm

37
Q

quadrantonopia

A

optic radiation / temporal lobe

38
Q

Patterns in spine nerve pathology

A

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
Q

Long tract signs

A

Associated with myelopathy

  • clonus: rapid contractions
  • upgoing plantars
  • hypertonic
  • Hoffman sign: flick middle finger
  • proprioception weakness
40
Q

L5 radiculopathy

A
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
Q

Cauda Equina syndrome

A

bilateral, pins+needles, bladder/bowel, saddle anaesthesia

42
Q

Thoracic metastases

A

commoner than disc degen.

= UMN in lower limb

43
Q

List the common types of brain tumours

A

1º:

  • GB multiforme (neuroepithelial tissue)
  • meningioma
  • adenoma (pituitary)

2º: mets

  • renal cell carcinoma
  • lung
  • breast
  • melanoma
  • GI
44
Q

Primary brain tumours

A

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
Q

Discuss the ways in which patients with brain tumours present clinically, including signs and symptoms by tumour site

A
  • ↑ICP = papilloedema, IIIn/VIn palsy
  • focal deficit
  • epileptic fits (tentorium lesions)
  • CSF obstruction
46
Q

Gerstmann’s Syndrome

A

Dominant parietal lobe lesions = calculating, self-awareness sensory

47
Q

Brain tumour investigation & management

A

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
Q

Tx of GBmultiforme

A

=> complete sx excision
=> steroids + anticonvulsants
=> RT, CT

49
Q

Commonest tumour types associated with cerebellum

A

Meningioma, arising from posterior cranial fossa

50
Q

factors that cause a raised ICP and the body’s physiological response to such an insult

A
  • straining, sneezing or getting up from recumbent position
  • sustained 20cmH20+ = pathology
  • significant impaired blood flow (hypoT, HT, hypoxia, ↑ICP) energy failure = cell death
51
Q

Munro-Kelly doctrine

A

Change in volume of contents or addition of new space occupying lesion increases pressure unless compensated by reduction of other content

52
Q

↑ICP Pathology

A

-focal/global ↓blood flow=↓energy=pump failure = cell dysfunction
= toxic metabolite = cell death

-

53
Q

pathophysiology of raised intracranial pressure and cushings reflex

A
↑ICP = triad
-HT
- irregular breathing
- bradycardia
as a response from cerebral ischaemia 
OR
brainstem distortion
54
Q

Cerebral Perfusion Pressure

A

Difference between MAP and ICP

55
Q

raised ICP results in a headache

A

prominent in morning d/t hypercapnic levels during the night s/t resp depression = vasodilation + ↓CSF abs.

56
Q

Role of autoregulation

A

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
Q

management increased intracranial pressure

A

=> monitoring of ICP with surgically implanted pressure transducer

=> CPP monitoring and optimising CPP to prevent insult

58
Q

Primary brain injury (focal and diffuse)

A
  • Diffuse axonal injury
  • diffuse oedema

-Herniation subtypes

59
Q

Understand secondary brain injury and cushings reflex

A

following injury, progressive neuro deterioration

glutamate=calcium= oedema 
NO = vasodilation
60
Q

Ischaemic injury

A

Wedge infarcts => areas more prone to damage, areas in between arterial supply

61
Q

State the different types and clinical features of head injury: Extradural, subdrual, subarachnoid haemorrhage

A

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
Q

investgiation and management of TBI

A

=> CT, MRI

=> maintaining ICP and follow-up

63
Q

intracranial aneurysms

A

aneurysm: thin wall vasc + hydroceph compl.; SUDDEN ONSET WORST HEADACHE

CoW ∴ central lesion in imaging