Transcript Cervical neurovascular dysfunction

REVISION OF CEREBELLAR
AND CEREBRAL DISORDERS &
ARTERIAL DEFICIENCIES
Caroline Peters
CEREBELLUM
2 hemispheres (3 lobes) / 1 vermis
1.
Coordination and correction of mvt via
cerebellothalamic tract
2.
Proprioception via ventral spinocerebellar tract
3.
Muscle spindles in trunk and Lex (Clarke’s column) via
dorsal spinocerebellar tract
4.
Balance via vestibulocerebellar tract
5.
Eye movements (same tract) CN III, IV, VI
Signs of cerebellar dysfunction
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Ataxia -  in postural co-ordination i.e. a stagger, falling
Intention tremor - evident before or during movement, but not at rest
Dysmetria - An inability to estimate distance correctly, e.g. on picking up an object,
i.e. there is oscillation around the goal and undershoot or overshoot of the target
Dysarthria - slow, slurred and explosive speech with pauses in the wrong places
Rebound Phenomenon - An inability to break movement
Dysdiadochokinesis - An inability to make rapid alternate movements
Decomposition of Movement – movements become jerky and irregular
A difficulty in performing complex actions involving simultaneous motion at more
than one joint.
Hypotonia - A decrease resistance to passive movement of limbs
Hyporeflexia – pendular
Difficulty in carrying out motor sequences that are usually automatic.
Oculo-motor disorders – nystagmus (an inability to fix a gaze)
Macrographia - Difficulty writing
Test the cerebellum
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Observation
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Position of the limbs
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Head deviated to one side
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Look for tremor
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Head bobbing
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Truncal ataxia (vermis dysfunction)
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Shifting of the feet / wavering unsteady?
Romberg’s Test – not a test of cerebellar dysfunction but a test of sensory ataxia
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Ask the patient to walk - Wide, staggering gait, resembles drunkenness = (B) cerebellar dysf
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Tandem Walking Test - It is the first function to be lost in alcoholic cerebellar cortical degeneration
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Head - Observe the eyes for nystagmus / head tilt
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Observe speech - Ask patient to say “la la la la la“ tests rapid movements of the tongue or “me me me me” tests
rapid movements of lips
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Upper & lower Extremities - Check tone and reflexes
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Dysdiadochokinesis - Thigh-slapping test / Finger to Thumb Test
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Test finger–nose–finger - Touch the pad of your index finger with the pad of his or her index finger.+ Hoffmann’s
sign
Heel–Shin Test - The right heel starts on the top of the left knee and slides down the shin to the foot.
Wallenberg syndrome
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= Lateral medullary ischaemia from occlusion of the
vertebral artery (or PICA)
nausea, vomiting and vertigo
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Ipsilateral features: Ataxia from cerebellar involvement. Horner's
syndrome from damage to descending sympathetic fibres.
Reduced corneal reflex from descending spinal tract damage.
Nystagmus.Hypacusis.Dysarthria.Dysphagia.Paralysis of palate,
pharynx, and vocal cord.Loss of taste in the posterior third of the
tongue.
Contralateral findings: Loss of pain and temperature sensation in
the trunk and limbs (anterior spinothalamic tract).Tachycardia and
dyspnoea (cranial nerve X).Palatal myoclonus (involuntary jerking
of the soft palate, pharyngeal muscles and diaphragm).
Cerebellar infarction
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Causes incoordination, clumsiness, intention tremor,
ataxia, dysarthria, scanning speech.
Early diagnosis is important, as swelling may cause
brainstem compression
BASAL GANGLIA
= collection of nuclei connected to thalamus, cerebrum and
brainstem (putamen, globus pallidus, caudate nuclei,
subthalamic nuclei, substantia nigra)
1.
Ordered 'background' movement
2.
Suppression of movement
3.
Initiate movement
4.
Phasic movement control - e.g. walking/arm swing
5.
'Autopilot’ movement - e.g. swimming
6.
Anti-gravity – esp. vestibulospinal
7.
Muscle tone - esp. reticulospinal
Signs of basal ganglia dysfunction
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NOT UMN LESION - Normal DOWNGOING plantar, No clonus, NOT
'clasp-knife' rigidity
Movement Disorders - often unilaterally initially
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Involuntary movements
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Tremor e.g. at rest (Parkinsonian)
Micrographia
Difficult to get going – akinesia
Reduced arm swing on walking  phasic movement
May affect posture / vestibulospinal
Chorea - 'dancing' – continuous rapid, jerky movements < Huntingdon’s, damage
to caudate/subthalamic/globus pallidus
Athetosis - slow writhing/snakelike < putamen
Hemiballismus - Violent, involuntary movement, ipsilateral and in proximal
joints < subthalamic nucleus damage
Rigidity - Cogwheel - hypertonia + tremor = intermittent resistance / Lead
pipe - Sustained resistance
Parkinsonism
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= progressive neurodegenerative disease, 2nd most
common after Alzheimer’s
Results from the degeneration of dopaminergic
neurons in the substantia nigra of the basal ganglia
in the midbrain
Clinically the disease becomes evident when
approximately 80% of the dopaminergic neurons
are lost
Parkinsons’s
Common Symptoms
 Hypokinesia –  motor activity
 Bradykinesia- slowness of movement
 Rigidity – lead pipe or cog-wheel
 Rest tremor
Clinical Signs
 Coarse rest tremor
 Pill-rolling movements (between thumb and index finger)
 Cogwheel rigidity
 Slowness of movement
 Speech is typically monotonous, soft, faint
 Expressionless face
 Small writing - micrographia
 Shuffling parkinsonian gait –  arm swing
Other movement disorders
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Putamen = athetosis
caudate, globus pallidus,
subthalamic = chorea
Subthalamic=
hemiballismus
(http://www.youtube.com/w
atch?v=hqg2GTUq1k4)
substantia nigra =
Parkinson’s disease
BRAINSTEM
Midbrain/ Pons/ Medulla (CN III to XII)
1.
Autonomic - not distinct anatomically, are associated with autonomic
centres in the hypothalamus
• Heart rate
• Blood pressure
• Ventilation
• Coughing and vomiting reflex
2.
Level of consciousness - and arousal
3.
Pain modulation - and site of descending analgesic pathways
4.
Habituation - Filters information so that not all input reaches the
cortex
5.
Extrapyramidal - neurons that influence the motor neurone pool of the
spinal cord i.e. muscle tone, posture etc..
Anatomy – brief overview
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Vertebral arteries – branching off subclavian, ascending though transverse foramina of the 6th
to 2nd vertebra, then sweeping laterally to enter trans foramen of C1 before going through
foramen magnum to form the basilar artery
Basilar artery divides into two post cerebral arteries at the upper pons (PICA)
Joined by the carotid and basilar systems they form the circle of Willis at the base of the
brain
Important points to consider when assessing clinically are:
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The cerebellum is supplied by branches from the basilar artery (long circumferential, posterior
cerebral, anterior inferior cerebellar and superior cerebellar arteries).
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The medulla is supplied by the posterior inferior cerebellar artery and by direct smaller
branches from the vertebral arteries.
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The pons is supplied by small and large branches from the basilar artery.
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The midbrain and thalamus are supplied by penetrating arteries from the posterior cerebral
arteries. The occipital cortex is perfused by the posterior cerebral artery.
1) Vascular dysfunction
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Atherosclerosis – most common, causing narrowing and
occlusion of large arteries. Only causes vertebrobasilar
ischaemia if BOTH vertebral arteries are stenosed at their
origin.
Embolic occlusion – fairly uncommon. Emboli can originate
from subclavian artery or aortic arch
Vertebral artery dissection (VAD) – usually in young
people presenting with severe occipital headaches and pain
in post nuchal region after head trauma
Carotid artery dissection (CAD) – more common than VAD.
Most common cause of stroke in middle-aged people,
typically presenting with neck pain and Horner’s syndrome
TIA’s
Carotid artery TIA - 90%:
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Contralateral motor and sensory disturbance
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Ipsilateral visual disturbanc
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Monocular blindness - if the TIA is in the ophthalmic artery territory
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There may be a carotid artery bruit in the neck
Vertebrobasilar Arterial Dysfunction / Disease - VAD’) 7% of TIA
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Vertigo
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Diplopia
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Dysarthria
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Weakness or sensory disturbance affecting one or both limbs
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Less commonly, impairment of vision, dysphagia
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Rarely, transient global amnesia, confusion, transient unconsciousness and  hearing
Lateral medullary ischaemia
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Result from occlusion of the posterior inferior cerebellar artery or partial occlusion of the basilar artery
or vertebral artery
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S/SS due to infection of the lateral medulla and inferior surface of the cerebellum
Cerebellar features:
 Ipsilateral limb ataxia
 Vertigo
 Nystagmus to the side of the lesion - due to damage to the vestibulo-ocular
connections
Brain stem features
 Sudden onset of dizziness and vomiting - due to the involvement of vestibular and
vagal nuclei respectively
 Dysphagia and dysarthria - due to lesion to the nucleus ambiguus and vagal nuclei
 Ipsilateral Horner's syndrome
 Ipsilateral facial sensory loss - pain and temperature
 Ipsilateral pharyngeal and laryngeal paralysis - cranial IX and X palsies
 Contralateral sensory loss - pain and temperature of the limbs and trunk
2) Locked-in syndrome
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Caused by infarction of the upper ventral pons.
Usually dramatic and sudden
quadriplegia with preserved consciousness
3) Weber’s syndrome
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Ventral midbrain affected
Ipsilateral mydriasis, cranial nerve III palsy and
ptosis.
Contralateral hemiplegia.
Intracranial bleed (STROKE)
Extradural/ Subdural/ Subarachnoid/
Intracerebral
1) Extradural – talk and die!
= results from rupture of one of the meningeal arteries that run between dura
and skull (middle meningeal artery is most common)
 Usual cause is skull fracture
 Effects develop rapidly, bleeding is arterial and at high pressure
 Commonly follows trauma to the temporal or temporo-parietal region
 Scalp oedema above the ear may be present
 Lucid interval - Concussion may be followed by temporary recovery of
consciousness for minutes or hours before the onset of drowsiness and
possibly coma – TALK & DIE
 Maybe ipsilateral, dilated pupil
 Bilateral CN III palsy as rising intracranial pressure > tentorial herniation
 There may be progressive contralateral hemiplegia
2) Subdural
= result from rupture of cortical bridging veins. These connect the extradural
venous system > the large intradural venous sinuses, blood fills the space
between the dura mater and arachnoid mater.
 Acute subdural haemorrhage < severe brain injury following trauma
 Chronic subdural haemorrhage < traumatic or may arise spontaneously
 Effects develop gradually < bleeding is venous in origin and low pressure
 Fluctuating conscious level
 There may be a history of gradual onset of
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Headaches
Memory loss
Personality change
Dementia, confusion
Drowsiness
3) Subarachnoid
= bleeding from intracranial vessels in the subarachnoid space
 Causes
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80% due to "congenital" / berry aneurysm (40 to 50 YOA)
10% due to other aneurysms – e.g. arteriosclerotic, traumatic
5% due to arteriovenous malformations
5% due to bleeding disease
Sudden severe headache ("my worst headache ever")
Headaches in the preceding weeks in 25 to 50%
Loss of consciousness or epileptic seizure occurs in 50%
Bigger bleeds may cause nausea, vomiting and convulsions
Focal signs, e.g. limb weakness, dysphasia may result from a haematoma
Presence of a CN III palsy
Papilloedema
Plantar responses are usually extensor
Back pain may arise from blood in the spinal theca
4) Intracerebral
= is bleeding into the brain substance with the
formation of a focal haematoma. Most commonly
due to hypertension, also trauma
 May rupture through cortical surface >
subarachnoid haemorrhage
 May rupture into ventricular system >
intraventricular haemorrhage
Cerebral lobes
Frontal Lobe
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Paralysis / paresis
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Mood changes / Changes in social behavior / Changes in personality
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Difficulty with problem solving / abstract thoughts
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Inability to express language < Broca's Aphasia
Parietal Lobe:
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Spatial neglect
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Agnosia – inability to recognize objects / speech / words etc..
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Problems with reading, writing and drawing
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 Mathematics (Dyscalculia)
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 Stereognosis
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 Graphesthesia
Occipital Lobes: Most posterior, at the back of the head.- Functions:
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Defects in vision fields
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Difficulty with locating objects in environment
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Visual hallucinations / illusions
Temporal Lobes
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Difficulty in understanding spoken words
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Short-term memory loss