Chapter 28: Trauma, Spinal Cord Injury, Cerebrovasc. Flashcards
Your patient describes how they’ve lost pain and temperature sense in both their arms, but they still know where their arms are in space and they can still discriminate pinpoint sensation. What is the site of the lesion?
Your patient comes to you two weeks after their initial visit, and now have a contracted pupil and a drooping eyelid. What’s happened?
What’s the last thing that your poor patient experiences?
Anterior white commissure. This is syringomyelia, in which a cystic degeneration of the spinal cord takes place between C8 and T1. The syrinx can expand to occlude the anterior white commissure, and cause the same symptoms.
The syrinx has expanded to occlude the lateral horn of the spinal cord, where the hypothalamospinal tract resides, at T1 . Now the patient has Horner’s syndrome, because this is the sympathetic tract to the face.
Muscle atrophy and fasciculations, as the syrinx expands to occlude the lower motor neuron.
What viral illness, spread by fecal oral transmission, then viremia, will present with the same symptoms as an autosomal recessive spinal degeneration? Also, name these illnesses.
Poliomyelitis will present with lower motor neuron signs , like flaccid paralysis, weakness with decreased muscle tone, impaired reflexes, and negative babinski sign.
Key here - degeneration of anterior motor horn.
Also degenerates in werdnig-hoffman disease, which is an inherited anterior motor horn degeneration. Floppy baby syndrome (remember botulism toxin?) , death a few year after birth.
You’re now in your neurology rotation. You have a patient present with hyperreflexia in the lower limbs and fasciculations in the lower limbs. What would be a key distinction between this disorder and syringomyelia?
This is amytrophic lateral sclerosis (ALS). You distinguish it from syringomyelia because you retain pain and temperature sense with ALS. Muscle atrophy is an early sign of ALS, and may present later in syringomyelia. It is a degeneration of the anterior motor horn (lower motor) and the lateral corticospinal tract (upper motor). Zn-CU SOD1 gene is mutated in familial cases, leading to excess free radical injury.
You’re evaluating a toddler, and you think your cell phone is buzzing on the table next to him. You ask the toddler to pick up the phone and tell you if it’s buzzing, and he tells you it isn’t, and hands it to you, missing your outstretched hand by a foot. You reach for your phone and it is, in fact, buzzing. It’s your attending, and he wants to know what your diagnosis is.
Friedrich’s ataxia. Loss of vibration and proprioception in due to multiple spinal cord tract degeneration, and degeneration of the cerebellum leads to ataxia.
This is an autosomal recessive disorder, due to an unstable trincuelotide repeat in frataxin gene - loss leads to more iron and more free radicals. Present in early childhood (leads to being wheelchair bound) and it’s associated with hypertrophic cardiomyopathy.
One of your professors is explaining at length the mechanism of a drug, when he becomes confused, and needs to sit down. Someone offers him a candy bar, which he eats. He regains his composure and completes the lecture. Later, he sees his primary care physician, who orders an ultrasound of the abdomen. What does he find, and what caused the confusion?
If he did not recover, what would he be at risk for?
Mild global ischemia can be caused by an insulinoma, which is a tumor of the pancreas oversecreting insulin (which his PCP might have found with the ultrasound Your professor has low blood sugar, and now his brain is hypoperfused.
Severe global ischemia, which can result in a vegetative state.
Upon autopsy, a medical examiner discovers a line of cortical necrosis of pyramidal cells in layers 3,5, 6 - what type of ischemia is this?
What is ischemic encephalopathy?
What is the cause of global ischemia?
moderate global ischemia - it will affect “watershed areas,” leading to infarcts in areas between anterior and middle cerebral arteries. Other types of damage you could experience are in the pyramidal cells of the hippocampus (long term memory) or in the purkinje layer of the cerebellum (integrates sensory perception with motor control).
Ischemic encephalopathy is widespread tissue damage from ischemia. Global ischemia is most often the result of cardiopulmonary arrest or extreme hypotension in severe shock.
You’re treating a patient whose chart says that he arrived yesterday at 6 PM with nystagmus. At 6 PM the present day, he tells you that his symptoms have remitted. But then you find out there was a charting error, and he actually arrived with symptoms at 5 PM yesterday, not 6. What does this change about your diagnosis?
If it was a focal deficit lasting for less than 24 hours, it’s a transient ischemic attack (TIA). If it’s for more than twenty four hours, it’s an ischemic stroke.
Nystagmus can be a sign of an ischemic stroke - look for a well defined deficit - a focal deficit.
Your patient has just experienced a car accident, and presents with normal consciousness, despite striking the steering wheel with his forehead with great force during the accident and fracturing the temporal bone of his skull . You sign off on his note, and come back to check on him the next day. He has expired. What blood vessel is implicated in his injury?
Middle meningeal artery - epidural hematoma. Once this artery is shorn, the patients may present with a “lucid period”, where they don’t experience symptoms of the injury, but can expire within 24-48 hours. The blood becomes a space filling lesion, causing herniation. You may see a lens shaped accumulation of blood along the suture lines - (the blood won’t cross the lines) between the dura and the skull).
You’re evaluating a high school football player who presents with progressive cognitive decline. He experiences headaches. After he returns to play against your wishes, he receives a minor hit, experiences a brain transtentorial herniation, and expires. On autopsy, the medical examiner finds extensive granulation tissue and fibrous tissue, with an inner and outer membrane. What was the initial mediator of injury?
Fibroblasts. This is a subdural hematoma, which could also result in reabsorption or calcification of the hematoma. With the head trauma, the dura moves with the skull, and the arachnoid moves with the cerebrum. The characteristic finding is a tearing of the bridging veins between the dura and arachnoid. The venous bleeding creates the hematoma.
After a brutal uppercut that spun his head to the right, Joe the boxer is knocked out for two minutes. Where is the dysfunction?
Disconnection between the cerebral hemispheres and the brainstem reticular formation. This is a concussion.
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You're examining the cerebral cortex of a patient who died of a stroke. Your attending asks you to determine whether the patient died of hemorrhagic or thrombotic cause. How could you tell?</p>
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Thrombotic strokes result from arteriosclerosis leading to tissue factor in the area leading to a thrombus directly in an artery feeding the cortex, resulting in a "pale infarct." Often at branch points. Hemorrhagic strokes would result from a clot being thrown by another location such as the left heart. The clot lodges in the circulation feeding the cortex, but then lyses, leading to ischemia and reperfusion. Usually middle cerebral artery. The cortex should look pale ("bland") if it's thrombotic, and dark if it's hemorrhagic.</p>
Your autopsy of a diabetic patient reveals cystic areas of scar tissue along the inner surface of the brain. What is the mechanism at work here?
What cognitive disorder would this patient have been at risk for?
Hyaline arteriosclerosis in patients with hypertension or diabetes leads to infarcts of the lenticulostriate arteries. These are then reabsorbed, leading to cysts that resemble lakes - lacunar strokes.
Multiple infarct dementia
You’ve been given a window to the pathological workings of a patient who has experienced an ischemic stroke. What is the pathological sequence of events - what would you see in one day, one week, and one month? What is the overall result?
First, red neurons (eosinophilic) develop in 12-24 hours. Then, coagulative necrosis with neutrophils and microglia (the macrophages of the brain). Finally, the formation of a fluid filled cyst surrounded by gliosis. This is all part of the process of liquefactive necrosis.
Your patient vomited in the ER after coming to visit with a severe headache. He goes into a coma after he’s admitted, and dies of a hemorrhage eventually found to be in the basal ganglia. What’s the name of the ruptured microaneurysms in this condition?
Charcot-Bouchard microaneurysms rupture following hyaline arteriosclerosis (hypertension) of the lenticulostriates leading to bleeding into the brain parenchyma. This is an intracerebral hemorrhage.
A patient with kidney disease is admitted to the hospital with the “worst headache of his life.” He has a stiff neck, but the CSF on lumbar puncture is sterile - it has a yellow tinge to it. What layer was missing from the anterior circle of Willis’ branch point with the anterior communicating artery?
What is a watershed infarct?
Media layer is missing at the branch point, causing a saccular outpouching known as a berry aneurysm. This leads to a subarachnoid hemorrhage, characterized by nuchal rigidity and the symptoms described in the question stem. It is associated with Marfan’s syndrome (connective tissue disorder) and polycystic kidney disease.
A watershed infarct is a distal region of overlapping major vessels, and very vulnerable to injury.
