Download Sudden Neurological Deficit

Sudden Neurological Deficit
1. Summarise the frequency, morbidity and mortality associated with cerebrovascular
disease in the community.
Frequency
: incidence 1.5/1000 overall  10/1000 at 75yo
Mortality
: 3rd cause of death in USA (after heart disease + cancer)
Morbidity
: 75% survive acute stage of stroke
60% have neurological deficit
20% mortality at 1 month, additional 5-10% after 1year
5. Summarise the factors that predispose to cerebrovascular disease.
Irreversible
Reversible
 Age
 Hypertension
 Gender (M>F, except in v. yg + v. old)  Heart disease ( HF, AF)
 Race (Afro-Caribbean > Asian >
 Diabetes
European)
 Hyperlipidaemia
 Heredity
 Smoking
 Excess alcohol consumption
 Polycythaemia
 Oral contraceptives
2. Describe the anatomy of the cerebral circulation, particularly the blood supply to the
major functional regions of the cerebral cortex, cerebellum and brain stem.
- 2 pairs of large vxls entering cranial cavity to supply the brain:
1. internal carotid aa. (branch off common carotid aa., enter thru carotid canal)
2. vertebral aa. (branch off subclavian aa., enter thru foramen magnum)
- vertebral arterial system  brain stem, cerebellum, occipital lobe, part of thalamus
carotids arterial system  the rest of forebrain
- circle of Willis provide collateral ‘safeguard’ to cerebral perfusion
- cortical supply:
1.Middle cerebral a. (MCA) supplies many deep structures + much of lateral cerebrum.
2.Anterior cerebral a. (ACA) supplies the ant. frontal lobe + medial aspect of hemisphere.
3.Posterior cerebral a. (PCA) supplies mainly occipital lobe, choroid plexus of 3rd + 4th
ventricles, and lower surface of temporal lobe.
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3. Outline the major sensory and motor descending pathways from the cortex to the
spinal cord.
Descending fibre systems (Motor)
System
Function
Origin
Ending
Cord Location
- Fine motor f(x)
(controls distal mm.)
- Modulation of
sensory f(x)
- Gross + postural
motor f(x)
( prox. + axial mm.)
Motor + premotor cx
Anterior horn cells
( interneurons+ LMN)
Motor + premotor cx
Ant. horn neurons
( interneurons+ LMN)
Vestibulospinal tract
- Postural reflexes
Lateral + medial
vestibular nucleus
Rubrospinal tract
- Motor f(x)
Red nucleus
Reticulospinal
Brain stem
reticular formation
Descending
autonomic
Tectospinal
- Modulation of
sensory transmission (esp. pain)
-Modulation of
spinal reflexes
- Modulation of autonomic f(x)
- Reflex head turning
Anterior horn interneurons + motor
neurons (extensors)
Ventral horn
interneurons
Dorsal + ventral horn
Lateral column
(crosses in medulla
at pyramidal
decussation)
Anterior column
(uncrossed until after
descend, when some
fibers decussate)
Ventral column
Medial longitudinal
fasciculus
- Coordination of
head + eye mov’t
Vestibular nuclei
Lateral corticospinal
tract (pyramidal)
Anterior corticospinal
tract
Hypothalamus,
brain stem nucleus
Midbrain
Ascending fibre systems (Sensory)
System
Function
Preganglionic autonomic neurons
Ventral horn interneurons
Cervical gray
Lateral column
Anterior column
Lateral column
Ventral column
Ventral column
Origin
Ending
Cord Location
Dorsal column
-Fine touch,
proprioception,
2-pt discrimination
Skin, joints, tendons
Spinothalamic tracts
- Sharp pain, temp.,
crude touch
Skin
Dorsal column
(cross in medulla at
lemniscal
decussation)
Ventrolateral column
Dorsal
spinocerebellar tract
- Movement +
position mechanism
Ventral
spinocerebellar tract
- Movement +
position mechanism
Spino-reticular
pathway
- Deep + chronic
pain
Muscle spindles,
Golgi tendon organs,
touch + P receptors
(via nucleus dorsalis)
Muscle spindles,
Golgi tendon organs,
touch + P receptors
Deep somatic
structures
Dorsal column nuclei
2nd order neurons
project to contralateral thalamus
Dorsal horn
2nd order neurons
project to contralateral thalamus
Cerebellar
paleocortex ( via
ipsilateral inferior
cerebellar peduncle)
Cerebellar paleo-cx
(via contra + ipsi sup.
cerebellar peduncle)
Reticular formation
Lateral column
Lateral column
Polysynaptic, diffuse
pathway in
ventrolateral column
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4. Compare and contrast the three common stroke syndromes: haemorrhagic, thrombotic and
embolic. In particular, outline the common syndromes that result from haemorrhage or
infarction in particular anatomical sites.
Causes
Sites
Clinical
Thrombotic Infarct
Usu thrombosis
superimposed on
atheromatous plaques
Embolic Infarct
Usu from heart :
thromboembolism
eg MI, AF, VHD;
carotid atheroma
Larger intracranial aa. , Smaller vessels,
important ones: internal Often in MCA territory
carotid a., vertebrobasilar system, MCA
Previous hx of TIA,
Develop very rapid
develop relatively late
(sec/min)
after attack (wks)
Haemorrhagic Stroke
Trauma, rupture
aneurysms,
vessels malformation.
Epidural, subdural,
subarachnoid,
intracerebral.
(refer objective 9)
Following trauma,
exertion   ICP
10. Describe the microscopic changes that occur in the brain as a result of ischaemia, and how
these changes differ from those found in other organs undergoing ischaemic necrosis.
Time Post
Infarction
8-12 hours
3-6 days
7-10 days
mths – yrs
Microscopic Pathology
Brain (Cerebral Infarct)
Other Organs eg. Heart (MI)
Red neuron
Oedema + haemorrhage
Few neutrophils
Myocyte hypereosinophilia
Liquefactive necrosis
Neutrophil infiltration
Coagulative necrosis
Lipid-laden macrophages
Disintegration of dead myocytes
( microglial )
Macrophage phagocytosis from
Reactive astrocytes
infarct border
Scattered blood vessels
Fibrovascular granulation tissues
Gliosis
Collagen deposition
Cyst with rim of glial fibers
collagen cellularity
+ macrophages
Dense collagen scar
7. Outline the common sequelae that result from cerebral infarction.
Immediate manifestation:
1. Focal neurological deficits
- resulting from death of tissue
2. Raised ICP
- from resultant oedema
3. Intracranial haemorrhage
- due to lysis of emboli, contributing to ICP
Manifestation mths/yrs later (particularly post-trauma):
1. Hydrocephalus
2. Dementia
3. Epilepsy
4. Brain tumours
5. Infectious disease 6. Psychiatric disorders
8. Summarise the effects of raised intracranial pressure.
Clinical features: headache, papilledema, vomiting, decreased consciousness,
slow-deep breath followed by Cheyne-Stokes respiration
Complications : herniation (subfalcine, transtentorial, tonsillar), hydrocephalus,
global cerebral hypoperfusion + death
(please refer Topic 21 Headache & Progressive Neurological Deficit, objective 2)
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6. Outline the major stroke syndromes that results form occlusion of the anterior,
middle and posterior cerebral arteries, as well as the effects of occlusion of the
vertebral artery and the perforating branches of the lenticulo-striate arteries.
Anterior cerebral artery occlusion
 UMN leg >arm
 Cortical sensory loss leg only
  UMN of the face, tongue, and upper limb (recurrent artery of Heubner)
  Ipsilateral anosmia (olfactory bulb + tract)
  Mental confusion + dysphasia (prefrontal cortex, cingulate gyrus, supplementary
motor area)
Middle cerebral artery occlusion
Infarction of middle third of hemisphere
 UMN face, arm> leg
 Homonymous hemianopia (genticul-calcarine tract)
  Global aphasia (if dominant lobe affected)
 Cortical sensory loss
Internal capsule infarct
 UMN CN VII, arm > leg
Posterior cerebral artery occlusion
Infarction of thalamus and cerebral cortex
 Hemianesthesia
 Homonymous hemianopia
  Memory deficit (hippocampal formation), transient if unilateral
but permanent of bilateral (space occupying lesion causing bilateral compression).
  Alexia (infarct in corpus callosum of dominant hemisphere).
Vertebral/ basilar artery occlusion
Thrombosis of the basilar artery
 Coma (infarction of reticular formation), decerebrate rigidity, and soon followed by
death due to respiratory centre failure.
 Bilateral divergence of eyes with fixed dilated pupils (CNIII disrupted).
 Wallenberg’s syndrome (lateral medulla infarction): loss of pain + temp ipsilaterally
in CNV distribution and contralaterally below neck; paralysis of mm. of soft palate,
pharynx and larynx on same side (nucleus ambiguus) causing dysphagia + dysarthria;
Horner’s syndrome; dizziness; cerebellar ataxia, nystagmus.
 Locked-in syndrome (ventral pons): paralysis of all voluntary movement except eyes.
Lenticulo striate occlusion
 Causes lacunar infarcts, which may be clinically silent, or cause severe neurological
deficits dependent on their extent + location.
 Occur in lenticular nucleus, thalamus, internal capsule, deep white matter, caudate
nucleus and pons.
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9. Describe the various types of intracranial haemorrhage, their common sites and
factors predisposing to their development.
Epidural
risks / causes severe trauma  fracture
common sites regions of temporal bone
potential space btwn skull + dura, where middle meningeal a. runs
pathology
torn meningeal vxls, usu a.  bld accumulation under arterial P 
separation of dura off inner skull surface  extradural haematoma
 uncontrolled arterial bld  brain compression  herniation
clinical
can be lucid for hrs btwn trauma + development of neurological signs
Subdural
risks / causes children (thinner vv.) with minor trauma
adults with brain atrophy (longer bridging vv.+ more space to move)
common sites lateral aspects of cerebral hemisphere
potential space btwn inner dural surface + outer arachnoid layer of
leptomeninges, where bridging vv. traverse
pathology
brain floats freely in CSF but fixed venous sinuses  minor trauma 
brain displacement tears bridging vv. at pts penetrating dura  subdural
bld  bld reabsorbed/ encapsulated/ calcified  may recur
clinical
manifest within 48hrs post injury, may have focal signs
but more often non-localising headache + confusion
Subarachnoid
risks / causes aneurysms: berry/ mycotic/ tubular/ traumatic/ dissecting aneurysms,
extension of traumatic bleed, intracerebral bleed into ventricular system,
vascular malformation, hematologic disturbances, tumours.
common sites (berry) 90% anterior circulation eg middle cerebral trifurcation,
circle of Willis, commonly at branch pts, infrequently post. fossa vxls.
pathology
- etiologic basis unknown, but with certain associations:
heritable systemic disorders, fibromuscular dysplasia of extracranial aa.,
coarctation of aorta, cigarette smoking + HT.
- spontaneous rupture or more often sudden ICP eg toilet strain
- arterial spasm (complication), can lead to ischaemic injury eg infarct
clinical
sudden ‘thunderclap’ headache (usu occipital) lasts hrs/days + vomiting,
LOC, photophobia, neck stiffness (6hrs), focal signs.
Intraparenchymal
risks / causes chronic hypertension - microaneurysm, amyloid angiopathy, systemic
coagulation disorders, vascular malformation, substance abuse.
common sites basal ganglia> thalamus> white matter > pons >cerebellum
pathology
1o hypertensive haemorrhage
chronic HBP  hyaline arteriosclerosis of small perforating vxls
(<300μm) microaneurysm (Charcot-Bouchard)  further BP 
ruptures, bleed + rapid ICP  remain small + becomes cystic defect /
more often extends into adjacent structures inc ventricular system
2o haemorrahge frequently occurs into regions of brain infarction
clinical
effects of mass lesion + raised ICP, focal neurological deficit.
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