1
Q
What is the main tract responsible for voluntary control of movement?
A
The pyramidal tract.
2
Q
Which tracts are included in the pyramidal tract?
A
The corticospinal tract and corticobulbar tract.
3
Q
What is the role of extrapyramidal tracts?
A
They provide indirect (involuntary) pathways for coordination of movement.
4
Q
What happens if the pyramidal tract is injured?
A
It causes UMN syndrome, which can result from strokes, tumours, trauma, infections, inflammation, demyelination, metabolic, or degenerative causes.
5
Q
What is the upper motor neuron (UMN)?
A
A motor neuron located in the brain or brainstem, whose axon travels down the spinal cord and innervates α and γ motor neurons in the ventral horn.
6
Q
What is the lower motor neuron (LMN)?
A
The α and γ motor neurons in the ventral horn of the spinal cord, whose axons travel peripherally to innervate muscle.
7
Q
Where does an UMN lesion occur?
A
In the brain, brainstem, or spinal cord before the synapse with the LMN.
8
Q
Where does a LMN lesion occur?
A
In the anterior horn cell, peripheral nerve, neuromuscular junction, or muscle.
9
Q
What are the hallmark features of an UMN lesion?
A
• Weakness
• Increased tone (spasticity)
• Increased reflexes (hyperreflexia)
• Clonus
• Upgoing plantar response (Babinski sign)
10
Q
What are the hallmark features of a LMN lesion?
A
• Weakness
• Decreased tone (flaccidity)
• Decreased reflexes (hyporeflexia/areflexia)
• Fasciculations
• Muscle wasting (atrophy)
11
Q
Why is stroke a common cause of UMN syndrome?
A
Because it often damages the corticospinal or corticobulbar tracts in the brain.
12
Q
What type of weakness does a stroke typically cause?
A
Contralateral hemiparesis (weakness on the opposite side of the body).
13
Q
A
14
Q
Why is the face often involved in a stroke affecting UMN pathways?
A
Because the corticobulbar tract supplies cranial nerves controlling facial muscles.
15
Q
A lesion in the cortex is called what?
A
A cortical lesion.
16
Q
A lesion in the corona radiata is called what?
A
A subcortical lesion
17
Q
A lesion in the internal capsule is called what?
A
A capsular lesion
18
Q
A lesion in the brainstem is called what?
A
A brainstem lesion.
19
Q
A lesion in the spinal cord is called what?
A
A myelopathy
20
Q
A lesion in the anterior horn cell is called what?
A
AHSD (anterior horn cell disease) or neuronopathy (e.g. MND, polio).
21
Q
A lesion in the nerve root is called what?
A
A radiculopathy.
22
Q
A lesion in the plexus is called what?
A
A plexopathy.
23
Q
A lesion in the peripheral nerve is called what?
A
A neuropathy
24
Q
A lesion at the neuromuscular junction (NMJ) is called what?
A
An NMJ disorder (NMJD), e.g. myasthenia gravis.
25
A lesion in the muscle itself is called what?
A myopathy.
26
Where are the cell bodies of the pyramidal tract concentrated?
Around the motor area of the cerebral cortex
27
Do the motor areas of the cerebral cortex control the same or opposite side of the body
The contralateral side of the body
28
Where are most UMN cell bodies of the pyramidal tract located?
In the precentral motor cortex (Brodmann area 4) and the premotor area (Brodmann area 6).
29
Besides areas 4 and 6, which other cortical regions also contain UMN cell bodies?
The supplementary motor area, primary somatosensory cortex, and superior parietal lobe
30
What is the motor cortex?
The region of the cerebral cortex responsible for planning, controlling, and executing voluntary movements.
31
Which hemisphere of the brain controls which side of the body?
Each hemisphere controls the contralateral side of the body (due to decussation of corticospinal fibres).
32
What are the main motor areas of the cortex?
• Primary motor cortex (M1, Brodmann area 4)
• Premotor cortex (part of area 6)
• Supplementary motor area (SMA, part of area 6)
33
Where is the primary motor cortex located?
On the precentral gyrus of the frontal lobe
34
What is its function? Primary motor cortex
Execution of precise, skilled voluntary movements (e.g. finger movements).
35
What is the motor homunculus?
A map in the primary motor cortex where different body parts are represented; areas needing fine motor control (face, hands) occupy more space.
36
Where is the premotor cortex located?
Anterior to the primary motor cortex, in the frontal lobe
37
What is its role? Premotor cortex
Planning and sequencing movements, especially those guided by external cues (e.g. catching a ball).
38
What happens if the premotor cortex is damaged?
Difficulty in performing movements in response to external stimuli, but basic strength remains intact.
39
Where is the SMA located?
On the medial surface of the hemisphere, anterior to the primary motor cortex.
40
What is its function? SMA
Planning complex, internally generated movements and coordinating movements involving both sides of the body.
41
What happens if the SMA is damaged?
Problems initiating movements, especially those requiring bilateral coordination.
42
Which other cortical areas contribute to motor control?
• Primary somatosensory cortex (areas 1, 2, 3): Provides sensory feedback for movement.
• Posterior parietal cortex (area 5 & 7, superior parietal lobe): Integrates sensory input with motor planning, important for spatial awareness.
43
What happens with a lesion in the primary motor cortex?
Contralateral weakness or paralysis, more severe in body parts with larger representation (face, hand).
44
What happens with a lesion in the premotor or SMA areas?
Apraxia – inability to perform learned, purposeful movements despite normal strength and coordination.
45
Why does a stroke in the internal capsule cause dense hemiplegia?
Because all corticospinal fibres converge there in a compact bundle, so a small lesion can knock out a large motor area representation.
46
What does “somatotopically organized” mean in the motor cortex?
Different body parts are represented in specific, organized areas of the motor cortex.
47
Where in the motor cortex is control of facial musculature located?
On the most lateral part of the cerebral hemisphere
48
Where in the motor cortex is control of the legs located?
On the most medial part of the cerebral hemisphere (along the interhemispheric fissure).
49
What is the “cortical homunculus”?
A distorted map of the human body in the motor cortex, where body parts are represented according to the degree of motor control needed, not actual size
50
Which body parts have the largest representation on the motor homunculus?
The face, lips, tongue, and hands, because they require fine motor control.
51
Where do upper motor neuron (UMN) axons of the corticospinal tract initially radiate and converge?
They radiate out into the corona radiata and converge at the posterior limb of the internal capsule.
52
Through which structures does the corticospinal tract descend after the internal capsule?
The tract descends through the cerebral peduncle in the midbrain, ventral pons, and the pyramids of the medulla.
53
What happens to most corticospinal axons at the inferior medulla?
The majority of axons decussate at the pyramidal decussation, continuing their descent contralateral to their cell bodies of origin.
54
After decussation, where do corticospinal axons enter the spinal cord?
They enter the lateral funiculus of the spinal cord, forming the lateral corticospinal tract.
55
Where do the lateral corticospinal tract axons terminate in the spinal cord?
They terminate throughout the ventral gray column and the base of the dorsal column.
56
How do lateral corticospinal axons controlling distal extremities differ from others?
They synapse directly on lower motor neurons, enabling fine motor control of fingers and hands, while others synapse on premotor interneurons.
57
What happens to about 10% of corticospinal axons at the pyramidal decussation?
They do not decussate and continue down the brain ipsilateral to their cell bodies, forming the anterior corticospinal tract.
58
What occurs to most anterior corticospinal tract fibers as they descend?
They decussate through the anterior white commissure before synapsing with interneurons
59
What is the role of the small percentage of corticospinal axons that do not decussate at all?
They control axial musculature, which is necessary for maintaining body posture.
60
Where do corticobulbar tract fibers originate?
From the motor cortex areas representing the face, primarily the lateral aspect of the motor cortex.
61
Through which structures do corticobulbar fibers descend?
They descend through the corona radiata and the internal capsule, similar to corticospinal tract fibers.
62
Which cranial nerves are primarily controlled by corticobulbar tract fibers?
CN V, VII, IX, X, XI, and XII, which control muscles of the face, jaw, pharynx, larynx, tongue, and neck.
63
How does upper motor neuron (UMN) innervation of cranial nerves generally occur?
Most cranial nerves receive bilateral UMN input, meaning each CN nucleus gets impulses from both hemispheres.
64
What is the functional significance of bilateral innervation in cranial nerves?
Unilateral CBT lesions usually produce mild weakness because the other hemisphere can compensate.
65
Which cranial nerves are exceptions to bilateral corticobulbar innervation?
CN VII (facial nerve) and CN XII (hypoglossal nerve)
66
What happens to the lower face if there is a UMN lesion of CN VII?
Contralateral lower face paralysis occurs, while the upper face is spared due to bilateral innervation
67
What is the effect of a UMN lesion of CN XII?
Contralateral genioglossus paralysis → the tongue deviates toward the opposite side of the lesion.
68
How does a lower motor neuron (LMN) lesion of CN XII differ from a UMN lesion?
LMN lesion → tongue deviates toward the same (damaged) side.
69
What LMN pattern helps localize lesions?
Weakness confined to a single nerve or root, or bilateral proximal muscles as seen in myopathy.
70
What is the classic UMN pattern of weakness?
Weakness of arm extensors and leg flexors, the so-called “anti-gravity” muscles, often seen in hemiparetic posture.
71
What pattern suggests a bilateral corticospinal tract lesion below the foramen magnum?
Weakness of all four limbs.
72
What pattern suggests a lesion in the cortex above the brainstem?
Weakness of the entire left side of the body, indicating corticospinal tract involvement above the decussation.
73
What pattern indicates a spinal cord lesion affecting the lower half?
Weakness of the entire lower half, lesion could be anywhere above the foramen magnum, especially if incomplete.
74
How does a lesion beyond the internal capsule present?
Weakness where the arm and face are less affected than the leg, because lateral fibers are affected and medial fibers are spared.
75
How does a lesion affecting medial corticospinal fibers present?
Weakness of one leg, as medial fibers supply the lower limb.
76
What is “crossed weakness” and what does it indicate?
Weakness of left lower motor neuron face and right hemiparesis → suggests lesion at the pontine nucleus of the facial nerve.
77
What additional neurological signs help localize lesions?
Higher functions, visual deficits, brainstem signs, sensory changes, cerebellar signs.
78
What are common causes of UMN/LMN patterns of weakness?
Causes include stroke, tumors, trauma, infection, inflammation, demyelination, metabolic disorders, degenerative diseases, and history is vital for localization.
79
Which higher cortical functions are distributed rather than localized?
Arousal, attention, memory, personality, and behaviour – these rely on networks across multiple brain regions.
80
Which higher cortical functions are localized?
Language, reading, writing, calculations, praxis, and visuospatial skills – these are linked to specific cortical areas.
81
What is a classic sign of a right cerebral cortical lesion affecting attention?
Left hemineglect – patient ignores the left side of space, often seen when drawing a clock face or copying objects.
82
How can left hemineglect be clinically tested?
Ask the patient to draw a clock, line bisection, or copy an object; they will omit the left side.
83
What type of visual field deficit occurs with post-chiasmal lesions?
Homonymous hemianopia – loss of the same half of the visual field in both eyes.
84
Which structures, if lesioned, can cause homonymous hemianopia?
Optic tract, optic radiations, or visual cortex on one side.
85
How does the visual field loss localize the lesion?
The deficit is contralateral to the lesion.
• Example: Left optic tract/radiation/cortex lesion → right homonymous hemianopia.
86
Can you give a simple way to remember post-chiasmal visual deficits?
“Lesion after the chiasm affects the opposite side of vision in both eyes.”
87
What do cranial nerves control?
Head and neck muscles, including eye movements.
88
How is cranial nerve and cerebellar control organized in terms of laterality?
Ipsilateral control – lesions produce deficits on the same side as the lesion.
89
90
Give an example of ipsilateral cranial nerve deficit
CN III palsy – if the lesion is on the right, the right eye shows the deficit.
91
What is the function of the lateral corticospinal tract?
Motor control, especially voluntary movement of limbs.
92
What is the function of the posterior (dorsal) columns?
Sensory – convey vibration, joint position sense (proprioception), and fine touch.
93
What is the function of the anterolateral (spinothalamic) tract?
Sensory – convey pain, temperature, and crude touch.
94
What is dissociated sensory loss and when does it occur?
Loss of pain and temperature sensation but preserved vibration and proprioception, or vice versa; occurs in spinal cord hemisection (Brown-Séquard syndrome).
95
What is the sensory pattern in Brown-Séquard syndrome?
• Ipsilateral loss: vibration, proprioception, fine touch, and motor function below the lesion.
• Contralateral loss: pain and temperature starting 1–2 levels below the lesion.
96
What is segmental sensory loss?
Loss of sensation in a dermatomal distribution, often due to nerve root or peripheral nerve lesions.
97
What is stocking-glove sensory loss?
Peripheral neuropathy pattern – distal extremities (hands/feet) are affected first; often bilateral and symmetrical.
98
What is cape distribution sensory loss?
Loss of sensation over shoulders and upper arms, typically seen in central cord lesions or syringomyelia.
99
What is the sensory pattern in a peripheral nerve lesion (e.g., carpal tunnel syndrome)?
Sensory loss confined to the distribution of a single nerve; often distal, unilateral, and focal.
100
What is the sensory pattern in a nerve root lesion (e.g., C6 radiculopathy)?
Sensory loss confined to a dermatomal distribution corresponding to the affected root.
101
What is the sensory pattern in polyneuropathy?
Symmetrical, distal loss of sensation (glove-and-stocking distribution), often affecting vibration, proprioception, and pain/temperature.
102
What is the sensory pattern in a complete spinal cord injury?
Bilateral loss of all sensory modalities below the lesion, depending on level of injury.
103
What is anterior cord syndrome?
Loss of pain and temperature below the lesion (spinothalamic tract) with preserved vibration and proprioception (posterior columns).
104
What is Brown-Séquard syndrome?
Hemisection of the spinal cord:
• Ipsilateral: motor, vibration, proprioception loss
• Contralateral: pain and temperature loss
105
What is central cord syndrome / syringomyelia?
Cape-like loss of pain and temperature over the shoulders and arms, sparing touch and proprioception.
106
What is the sensory pattern in a brainstem injury?
Crossed sensory loss – ipsilateral cranial nerve sensory deficits with contralateral body sensory deficits.
107
What patterns of weakness suggest a cortical lesion?
• Differential weakness: face and arm > leg (or leg > face/arm)
• Other features: hemianopia, aphasia, hemineglect, cortical or primary sensory loss, cognitive dysfunction
108
How does a corona radiata lesion present?
• Differential weakness: arm/face >> leg or leg >> arm/face
• Other features: primary sensory loss
109
How does a lesion of the internal capsule present?
Dense weakness: face = arm = leg on the contralateral side
110
How does a brainstem lesion present?
• Dense weakness: arm = leg (contralateral)
• Other features: cranial nerve signs (esp eyes/bulbar), crossed signs, cerebellar signs
111
How does a spinal cord lesion present?
• No face involvement
• Spastic para- or quadriparesis
• Sensory level
• Sphincter involvement
112
Which part of the body is most affected in ACA territory ischaemia?
Leg and foot, because the ACA supplies the medial portion of the motor and sensory cortex.
113
Why does ACA ischaemia primarily affect the leg?
The medial surface of the cerebral hemisphere (paracentral lobule), which controls the lower limb, is supplied by the ACA.
114
Which cerebral artery is most commonly affected by stroke?
Middle cerebral artery (MCA).
115
Which areas of the body are typically affected in MCA stroke?
Face and arm weakness > leg weakness, because the MCA supplies the lateral part of the motor and sensory cortex.
116
What other deficits can occur in MCA territory stroke?
• Aphasia (if dominant hemisphere affected)
• Neglect (if non-dominant hemisphere affected)
• Gaze deviation toward the side of the lesion
• Contralateral homonymous hemianopia
117
Which areas are supplied by the posterior cerebral artery (PCA)?
Occipital lobe, inferomedial temporal lobe, and parts of the thalamus and midbrain.
118
What is the classic visual deficit in PCA stroke?
Contralateral homonymous hemianopia, sometimes with macular sparing.
119
What other deficits can occur in PCA territory stroke?
• Thalamic sensory loss if thalamic branches are affected
• Memory impairment if medial temporal lobe is involved
• Alexia without agraphia if dominant occipital and splenium are involved
120
What is the Bamford stroke classification used for?
To categorize ischaemic strokes based on clinical presentation and localization.
121
What are the main categories of the Bamford classification?
1. TACI – Total Anterior Circulation Infarct
2. PACI – Partial Anterior Circulation Infarct
3. LACI – Lacunar Infarct
4. POCI – Posterior Circulation Infarct
122
Features of TACI (Total Anterior Circulation Infarct)?
All three of the following:
• Contralateral motor and/or sensory deficit of face, arm, and leg
• Homonymous hemianopia
• Higher cerebral dysfunction (aphasia, neglect, visuospatial disorder)
123
Features of PACI (Partial Anterior Circulation Infarct)?
Only two of the TACI features, or isolated higher cortical dysfunction (e.g., aphasia, neglect).
124
Features of LACI (Lacunar Infarct)?
Small subcortical infarcts with one of the classic syndromes:
• Pure motor stroke
• Pure sensory stroke
• Sensorimotor stroke
• Ataxic hemiparesis
No cortical signs (no aphasia, neglect, or visual field loss).
125
Features of POCI (Posterior Circulation Infarct)?
Infarcts in vertebrobasilar territory with any of:
• Cranial nerve palsy with contralateral motor/sensory deficit
• Bilateral motor/sensory deficits
• Cerebellar signs
• Isolated homonymous hemianopia
126
What is spasticity in UMN syndrome?
A velocity-dependent increase in muscle resistance to passive stretch; slow stretches do not cause resistance, but brisk stretches cause abrupt resistance followed by a decrease (clasp-knife phenomenon).
127
Which muscles are most affected by spasticity in UMN syndrome?
Antigravity muscles:
• Flexors of the arms
• Extensors of the legs
128
Why do patients with UMN syndrome often exhibit flexor and extensor spasms?
Because of decreased modulation of spinal reflexes by descending pathways.
129
What is clonus?
A sequence of rhythmic, involuntary muscle contractions (5–7 Hz) in response to abrupt stretch stimuli; commonly seen at the ankle.
130
How can clonus be elicited?
• Brisk dorsiflexion or plantarflexion at the ankle
• Sometimes during voluntary movement or cutaneous stimulation
131
What causes hyperreflexia of deep tendon reflexes in UMN syndrome?
Decreased modulation by descending inhibitory pathways, leading to abnormally brisk reflexes and radiation of reflexes (e.g., tapping the supra-patellar tendon elicits a knee-jerk reflex).
132
What happens to superficial reflexes in UMN lesions?
They are decreased or abolished, e.g.:
• Superficial abdominal reflex: tensing of the abdominal muscles when stroking the skin
• Cremasteric reflex: elevation of the scrotum when stroking the medial thigh
133
What is pseudobulbar palsy?
Bilateral UMN damage to cranial nerves (mostly with bilateral innervation) causing:
• Slurred speech
• Dysphagia
• Dysarthria
• Brisk jaw jerk
• Spastic tongue
• Pseudobulbar affect
134
Which cranial nerves are exceptions to bilateral UMN innervation?
CN VII (lower face) and CN XII (tongue) – receive unilateral innervation from the pyramidal tract.
135
What are the clinical features of a unilateral UMN lesion of CN VII or CN XII?
• CN VII: contralateral lower facial droop
• CN XII: contralateral tongue deviation (tongue deviates away from the lesion)
136
What is spinal shock?
Acute period after spinal cord injury with:
• Flaccid paralysis
• Hypotonia and hyporeflexia (most evident in limbs)
• Truncal muscles usually preserved
• Duration: days to weeks, after which spasticity and hyperreflexia develop
137
Nondumiso has isolated left arm and hand weakness, but speech, sensation, vision, and language are normal. How is this classified?
Right Lacunar stroke (LACS) – isolated motor deficit without cortical signs.
138
Pieter has right-sided face and arm weakness, cannot see to his right, and has dysphasia. How is this classified?
Left Total Anterior Circulation Infarct (TACI) – weakness + homonymous hemianopia + higher cortical dysfunction.
139
Jan has vertigo, diplopia, and cerebellar signs but no weakness. How is this classified?
Posterior Circulation Infarct (POCI) – brainstem/cerebellar signs without anterior circulation cortical deficits.
140
Cynthia has a clumsy, weak left hand and slurred speech, otherwise normal. According to Bamford classification, what subtype is this?
Right Partial Anterior Circulation Stroke (PACS) – some cortical signs (speech), but not all features of TACI.
141
According to Bamford (OCSP) stroke outcomes, which statement is FALSE?
* A) Two-thirds of partial anterior circulation strokes (PACS) can function independently at 6 months.
* B) Total anterior circulation strokes (TACS) have a mortality rate >50% at 6 months.
* C) Posterior circulation strokes have the highest risk of early stroke recurrence.
* D) Roughly one in four lacunar strokes have significant disability at 6 months.
Answer: C is FALSE – posterior circulation strokes do not have the highest risk of early recurrence; lacunar strokes have a lower recurrence risk compared to cortical strokes.
142
Pieter has right-sided face and arm weakness, cannot see to his right, and has dysphasia. According to Bamford classification, what subtype is this?
Left Total Anterior Circulation Stroke (TACS) – presence of weakness + homonymous hemianopia + higher cortical dysfunction.
143
Regarding higher cerebral functions, which is least useful for localizing weakness?
Level of arousal – it is distributed, not localized; aphasia, neglect, and apraxia are more localized.
144
Nondumiso has isolated left arm and hand weakness with normal speech, sensation, vision, and language. Bamford classification?
Right Lacunar Stroke (LACS) – isolated motor deficit without cortical signs.
145
Regarding clinical localization of weakness, which statement is accurate?
o Cranial nerve abnormalities are usually seen ipsilateral to the lesion in association with
ipsilateral limb weakness.
o In the lateral medullary syndrome, unilateral weakness of arm and leg and contralateral
cerebellar signs may be found.
o Weakness of face and arm greater than the leg is characteristic of injury to the
corticospinal tract above the internal capsule.
o When aphasia is present with hemiparesis, the right cortex is typically involved.
Weakness of face and arm greater than leg is characteristic of injury to the corticospinal tract above the internal capsule.
146
Mohamed has a left homonymous hemianopia but no motor or sensory signs. According to the
Bamford stroke classification, what sub-type is this classified as?
o Right Lacunar stroke (LACS)
o Right Posterior circulation stroke (POCS)
o Right Total anterior circulation stroke (TACS)
o Right Partial anterior circulation stroke (PACS)
Right Posterior circulation stroke (POCS)
147
148
Regarding the anatomy of upper motor neuron weakness, which of the following is TRUE?
o The corticospinal cell bodies are located in the anterior horn of the spinal cord.
o The corticospinal tract decussates in the upper medulla.
o The primary motor cortex is located anteriorly to the central sulcus.
o Lesions of the anterior corticospinal tract result in weakness of the contralateral side of the
body.
The primary motor cortex is located anteriorly to the central sulcus
149
Regarding an injury to the corticobulbar tracts, which of the following statements is INCORRECT?
o Corticobulbar tracts from the medial motor cortex innervate the contralateral lower facial
muscles.
o Bilateral injury to corticobulbar tract fibres causes a pseudobulbar palsy.
o Corticobulbar tracts supply bilateral cranial nerves which control muscles of face and neck.
o Injury to corticobulbar tract fibres innervating the twelfth cranial nerve result in deviation of
the tongue towards the contralateral side.
Corticobulbar tracts from the medial motor cortex innervate the contralateral lower facial
muscles.
150
Which strokes are suitable for thrombectomy?
Large vessel strokes (e.g., MCA, ICA), not lacunar strokes (small vessel).
151
What are the cardioembolic causes of thromboembolic strokes?
Emboli from the heart due to:
• Atrial fibrillation (warfarin reduces risk by 70%)
• Endocarditis (mitral/aortic valves)
• Abnormal heart valves
• Dilated cardiomyopathy
• Myocardial infarction with akinetic wall segments
152
What are vascular and atherosclerotic causes of thromboembolic stroke?
• Carotid atherosclerosis
• Vasculitis (large, medium, small vessels) – infective: syphilis, TB, HIV, VZV
• Smoking (accelerates atherosclerosis, worsened by HIV)
153
What factors are important in younger patients with stroke?
Virchow’s triad:
• Blood constituents: prothrombotic states (protein C/S deficiency, antithrombin III, factor V Leiden)
• Vessel wall: carotid abnormalities
• Stasis: heart issues, shunts, patent foramen ovale
154
What are common venous thrombotic causes of stroke?
• Rare compared to arterial strokes
• Prothrombotic states: pregnancy, contraceptives, cancer, TB
• Antiphospholipid antibodies – cause both venous and arterial thrombosis, associated with miscarriages
155
What modern interventions are available for acute stroke?
• Thrombectomy to remove clots from large vessels
• Stenting of cerebral arteries
• These treatments can be dramatic with excellent outcomes.
156
What determines outcome after stroke?
Recanalization – reopening blocked vessels quickly improves survival of brain tissue.
157
How do strokes evolve over time?
• Stroke develops over days, providing a variable intervention window
• Maintaining homeostasis improves outcomes:
• Blood pressure
• Blood glucose
• Bladder and bowel function
158
What happens in the core and penumbra during an acute stroke?
• Core: areas with no collateral supply die first
• Penumbra: areas with reduced blood flow malfunction, giving early neurological signs but are salvageable if perfusion is restored
159
How does collateral circulation affect stroke progression?
• Good collaterals → slower progression, “fast progressors” can be treated successfully
• Large blocked areas with poor penumbra → less benefit from thrombolysis, as much tissue is already infarcted
160
Mohamed has left homonymous hemianopia but no motor or sensory signs. Bamford classification?
Right Posterior Circulation Stroke (POCS) – visual deficit only, no cortical motor/sensory signs.
161
Regarding the anatomy of upper motor neuron weakness, which of the following is TRUE?
o The corticospinal cell bodies are located in the anterior horn of the spinal cord.
o The corticospinal tract decussates in the upper medulla.
o The primary motor cortex is located anteriorly to the central sulcus.
o Lesions of the anterior corticospinal tract result in weakness of the contralateral side of the
body.
The corticospinal tract decussates in the upper medulla.
162
Regarding an injury to the corticobulbar tracts, which of the following statements is INCORRECT?
o Corticobulbar tracts from the medial motor cortex innervate the contralateral lower facial
muscles.
o Bilateral injury to corticobulbar tract fibres causes a pseudobulbar palsy.
o Corticobulbar tracts supply bilateral cranial nerves which control muscles of face and neck.
o Injury to corticobulbar tract fibres innervating the twelfth cranial nerve result in deviation of
the tongue towards the contralateral side.
Corticobulbar tracts from the medial motor cortex innervate the contralateral lower facial muscles.
163
Which strokes are suitable for thrombectomy?
Large vessel strokes (e.g., MCA, ICA), not lacunar strokes (small vessel).
164
What are the cardioembolic causes of thromboembolic strokes?
Emboli from the heart due to:
• Atrial fibrillation (warfarin reduces risk by 70%)
• Endocarditis (mitral/aortic valves)
• Abnormal heart valves
• Dilated cardiomyopathy
• Myocardial infarction with akinetic wall segments
165
What are vascular and atherosclerotic causes of thromboembolic stroke?
• Carotid atherosclerosis
• Vasculitis (large, medium, small vessels) – infective: syphilis, TB, HIV, VZV
• Smoking (accelerates atherosclerosis, worsened by HIV)
166
What factors are important in younger patients with stroke?
Virchow’s triad:
• Blood constituents: prothrombotic states (protein C/S deficiency, antithrombin III, factor V Leiden)
• Vessel wall: carotid abnormalities
• Stasis: heart issues, shunts, patent foramen ovale
167
What are common venous thrombotic causes of stroke?
• Rare compared to arterial strokes
• Prothrombotic states: pregnancy, contraceptives, cancer, TB
• Antiphospholipid antibodies – cause both venous and arterial thrombosis, associated with miscarriages
168
What modern interventions are available for acute stroke?
• Thrombectomy to remove clots from large vessels
• Stenting of cerebral arteries
• These treatments can be dramatic with excellent outcomes.
169
What determines outcome after stroke?
Recanalization – reopening blocked vessels quickly improves survival of brain tissue.
170
How do strokes evolve over time?
• Stroke develops over days, providing a variable intervention window
• Maintaining homeostasis improves outcomes:
• Blood pressure
• Blood glucose
• Bladder and bowel function
171
What happens in the core and penumbra during an acute stroke?
• Core: areas with no collateral supply die first
• Penumbra: areas with reduced blood flow malfunction, giving early neurological signs but are salvageable if perfusion is restored
172
How does collateral circulation affect stroke progression?
• Good collaterals → slower progression, “fast progressors” can be treated successfully
• Large blocked areas with poor penumbra → less benefit from thrombolysis, as much tissue is already infarcted
173
What is the first step if acute stroke is suspected (ROSIER scale >0)?
Maintain plasma glucose, hydration, oxygen saturation, and temperature within normal limits.
174
What imaging is required to differentiate between ischaemic and haemorrhagic stroke?
Non-contrast CT scan.
175
What are the treatment options for ischaemic stroke if onset is <4.5 hours?
Thrombolysis with tPA (e.g., Alteplase) if no contraindications
Consider thrombectomy
After 24 hours, exclude haemorrhagic transformation on CT head and give aspirin 300 mg
176
What is the management of ischaemic stroke if onset is >4.5 hours?
Consider thrombectomy
Give aspirin 300 mg
177
What are the indications and time windows for mechanical thrombectomy?
Recommended if modified Rankin scale <3 and NIHSS >5
Offer if <6 hours of onset with confirmed proximal anterior circulation occlusion
Offer if 6–24 hours of onset with confirmed proximal anterior circulation occlusion and salvageable brain tissue
Consider if <24 hours of onset with confirmed proximal posterior circulation occlusion
178
What is the management for haemorrhagic stroke?
Reverse anticoagulant
Aim to maintain BP <140/80 mmHg
Refer for neurosurgical assessment
Neurology
flashcards
Decks in class (38)
# Cards
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Headache113
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Headache cases13
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Weakness59
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Epilepsy131
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The Rule of 4 and Brainstem Localisation36
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Epilepsy133
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Into To Neuro51
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Raised ICP102
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Epilepsy CPC31
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Stroke178
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Movement Disorders93
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Stroke39
-
Traunatic Brain Injury90
-
Glascoma Scale13
-
CNS Tumors115
-
Neuroradiology156
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Neurocascular43
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Neurosurgery Red Flags93
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Surgical Stroke38
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The Spine29
-
Spinal Pathology103
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Spinal Cord Compression30
-
Spinal Lesion88
-
Spina Bifida83
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Neuro Exam33
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Spinal Quiz26
-
Stroke Localisation45
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Chronic Dizziness62
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Coma63
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Denentia125
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Disorders Of The Spinal Cord132
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Hyperkinetic Movements154
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Hypoxic Ischemic Brain Injury20
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Infections Of The Nervous System77
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Motor Neuron Disease38
-
Muscle Disease33
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Peripheral Berve Disease37
-
Spinal Cord Lesions44
