ANATOMY - STROKE Flashcards
When 60 y/o woman was in her late-40’s, she visited her GP for advice on menopause. O/E: hypertensive and suffering from hypercholestrolaemia. Some of her older relatives had been diagnosed with these problems in the past. Since being placed on daily treatment for these conditions, and having made the changes to her lifestyle that her GP recommended, she has been reasonably well. One morning while doing her shopping, she felt faint, felt lameness in her right arm and leg, and then fell over. Paramedics noticed that her speech was slurred. On arrival at the Casualty Unit BP was 160/90 and PR was regular at 110 beats per minute. O/E: severely slurred speech and the flaccid weakness of the right arm and leg, as well as weakness of the muscles of facial expression on the right side of her face. She could, however, wrinkle her forehead on both left and right sides.
Urinalysis revealed 1+ protein (N = -ve), 2+ glucose (N = -ve), blood –ve (N = -ve), ketones –ve (N = -ve), pH 5.5 (N = diet dependent). Plasma glucose (non-fasting) was 10.0mmol/l (N = 4-8), and C-reactive protein 45mg/l (N = 0-5mg/l).
Patient’s facial paralysis and speech improved rapidly over the next few days, but her leg and arm recovered much more slowly.
On which side of the cerebrum did the patient suffer a CVA? Motivate your answer by naming the spinal tract involved and by describing its course (2)
CVA on left side – corticospinal tract crosses the midline (pyramidal decussation) to supply the contralateral side of the body.
Name the cranial nerve that supplies the muscles of facial expression. Explain why the patient retained the nerve supply to the muscles of her forehead, yet suffered weakness of the muscles of facial expression on her lower right side (2)
L & R VII provide bilateral supply to the upper 1/3 and unilateral (contralateral) supply to the lower 2/3 of the face.
Upper motor neuron damage is characterised by a spastic paralysis in the limbs. Explain why the patient presented with weakness of her arm and leg musculature in the case scenario (2)
Immediate effect of UMN damage is flaccid paralysis. Fibres coming from the cortex supplying these regions are affected. After 5-7 days, classic spastic paralysis sets in.
Explain why the patient felt faint (2)
Left brain cerebrovascular accident (affecting left hemisphere motor, and/or premotor, frontal lobe cortical areas) impairing blood flow to left hemisphere thereby decreasing oxygen and glucose supply to neural tissue, impairing brain function, causing dizziness and feeling faint.
Explain why the patient felt lameness in her right arm and leg and not her left arm or leg (5)
The lateral corticospinal tract that innervates motor neurons that control muscles in the arm and leg on the right side of the body originates in the left premotor, motor and somatosensory cortex. 80% of the fibres in the corticospinal tract cross the midline in the pyramidal decussation of the medulla oblongata and descend in the dorsal part of the lateral column (dorsolateral column) to synapse onto lower motor neurons in the ventral horn of the spinal cord, thereby stimulating muscles on the contralateral side of the body. In contrast, the ventral corticospinal tract terminates bilaterally on lower axial motor neurons that control movement of the neck and trunk.
The fact that the patient’s speech was slurred provided information concerning the location of the malfunction. Explain what you can deduct from this observation (2)
Control of movements required for speech is localized in Broca’s area, in the left frontal lobe, suggesting occlusion of the left middle cerebral artery. Slurred speech also suggests upper motor neuron (UMN) damage in precentral gyrus of left or right frontal lobe impairing control of tongue by the hypoglossal nerve (CN XII) which innervates the tongue bilaterally but only weakly ipsilaterally.
What could have caused the weakness of facial expression on the right side only of the patient’s face? Why was the left side not equally affected? (2)
This suggests that corticobulbar fibres are affected i.e. damage to UMNs that innervate LMNs in the brain stem, in this case the facial nerve (CN VII). Motor neurons that innervate the lower part of the face receive input from predominantly contralateral areas of the brain. Please note that the corticobulbar fibres decussate in the brain stem to influence LMNs either unilaterally or bilaterally. The lower left side of the face is innervated by the left CN VII (facial nerve) which receives input from the right upper neuron that projects its axon in the corticobulbar tract.
Explain why the patient’s facial paralysis and speech improved within a few days whereas her leg and arm recovered much more slowly (1)
Her facial paralysis and speech impairment improved within a few days suggesting that the UMNs in the corticobulbar tract were probably compromised by transient compression due to oedema (surrounding haemorrhage or ischaemia) which cleared up within a few days. The UMNs in the lateral corticospinal tract appear to have undergone more severe ischaemic changes.
45 y/o man has recently cut back from smoking about 30 cigarettes a day to less than 10 cigarettes a day, and reports being a moderate drinker of alcohol for most of his adult life. Began exercising daily. While cycling at the gymnasium one evening, he suddenly experiences a dull pain in his head and feels nauseous. Feels a dragging weakness and numbness on the right side of his body. Speech is slurred. Left side of his face seems to be smooth and does not wrinkle, that his left eye does not close fully when he O/E: suffering from a flaccid paralysis on the right side of his body and weakness of the entire left side of his face.
Draw and label a diagram that you could use to explain to this patient how the affected part of the brain (brainstem specifically) is supplied by blood vessels (7)
Cerebral arterial circle – contributions from paired internal carotid and paired vertebral arteries – perforating branches to brainstem – (an informed student may suggest that a vessel to the pons is occluded.)
Explain why this patient experiences “the dragging weakness and numbness on the right side of his body” as well as the “paralysis of the left side of the face?” (4)
The patient has a CVA with the lesion at the level of the PONS [1]. The lesion at this level affects the facial nucleus as well as the pyramidal tract [1]. The LMN which originates at this level supplies the ipsilateral face, hence the facial paralysis [1]. Pyramidal tract fibres passing through this area are also affected, however they are still uncrossed and hence the contralateral limbs/side of the body will be affected [1]
The weakness in the left of his face is caused by a lesion affecting CN vii which has its nucleus on the ipsilateral side in the pons and the weakness on the right side of his body is caused by a lesion anywhere along the spinothalamic tract [corticospinal tract?] which runs from the left motor cortex and decussates in the caudal medulla where it runs down contralaterally as the spinal lemiscus. Therefore the blockage must have occurred at a point which cuts off blood supply to an area where these two tracts overlap.
Why does this patient present with a flaccidity of the facial and limb musculature, and how will these signs change after a short time? (2)
Initially, brain represses all nerve input as a protective mechanism, but later on Upper Motor Neurone signs will then become evident – hypertonia, hyperreflexia, spasticity.
The facial and limb musculature will eventually become spastic as per usual with an UMN lesion. They are initially flaccid?
