Monday, July 13, 2009

Case Study - 49.

A 74-year-old retired lawyer was brought into a small community clinic in northern Maine complaining of a pain on the right side of his head and weakness on the left side of his body.

He had had mild hypertension for several years but was otherwise in excellent health. He had been in
Maine on a hunting trip for the previous 3 days. On the day of admission he had been walking back to camp in a heavy snowfall when he suddenly developed pain behind the right ear, along with weakness of the left side of his body and dysarthria.

He was brought immediately to the clinic, where he was examined by a physician's assistant. He was observed to be afebrile, to have a pulse rate of 88 beats per minute, regular breathing at a rate of 16 respirations per minute and blood pressure of 200/112 mmHg. He was awake, orientated, and followed commands.

He was dysarthric and complained of a steady, moderately severe pain above and behind the right ear. His head and eyes deviated moderately to the right, and there was a left homonymous hemianopsia.

The patient denied any recent history of trauma, headaches, or dizzy periods. He admitted to consuming one to two bottles of beer each evening on the hunting trip but denied consistent use of alcohol in his daily life. He also denied the use of any illicit drugs and was not taking any prescription medications.

He was able to deviate his eyes just past the midline to the left, volitionally; however, with the doll's head manoeuvre, his eyes could be directed into the left visual hemisphere. The pupils were unequal, the right being 2 mm and the left, 3 mm; both reacted to light. Sensation was reduced in the left side of the face and cornea.

There was a moderately severe, flaccid left hemiparesis interrupted intermittently by clonic movements of the leg and tonic flexor movements of the left arm. Stretch reflexes on the left side were reduced, but the plantar response was extensor.

Within an hour of admission, the patient was having periodic decorticate posturing on the left side. The right plantar response had become extensor. He gradually lost consciousness; within 4 hours of admission he was unresponsive except to noxious stimuli.

At first, painful stimuli produced extensor responses on the left but decorticate responses on the right; however, this pattern finally matured into bilateral extensor posturing, slightly more pronounced on the left than on the right.

By this time, the right pupil had dilated and fixed in an oval shape, being 7 mm vertically and 3 mm horizontally. Minimal oculomotor responses could be elicited to cold caloric stimulation, and the patient was hyperventilating. Blood pressure had risen to 235/150 mmHg.

One hour after entering the clinic, preparations were begun for emergency transfer to Bangor, Maine, the closest major medical centre, however, because of the snowstorm, air travel was impossible and ground transportation was slow.

Treatment with mannitol was started, and during the next hour the patient's condition stabilized, except that the right pupil became round and regained a minimal reaction to light. En route to
Bangor, the patient's blood pressure dropped to 160/60 mmHg, he began to vomit, and his temperature rose to 39.6 degrees centigrade.

He began to sweat profusely, and within 6 hours of initial presemnation at the clinic, the decerebrate responses had become less intense, the pupils were fixed, slightly irregular at 3 to 4 mm in diameter, and unequal, oculocephaic responses were absent, and respiration was quiet and shallow.

Within 8 hours of admission to the clinic (2 hours into the trip to
Bangor), respiration was ataxic, the pupils remained slightly unequal, with no oculovestibular responses; and the patient was diffusely flaccid but had bilateral extensor plantar responses and mild flexor response in the legs to noxious stimulation of the soles of hte feet. He died 30 minutes later while still en route.
 
QUESTIONS
 
1. Does the patient exhibit a language or memory deficit or an alteration in consciousness or cognition?
 
2. Are signs of cranial nerve dysfunction present? If so are they signs of segmental or supersegmental dysfunction?
 
3. Are there any changes in motor functions, such as reflexes, muscle tone, movement, or coordination? If so are they signs of segmental or supersegmental dysfunction?
 
4. Are any changes in sensory functions detectable?
 
5. Based on the answers to the above questions, at what level in the neuraxis is this lesion most likely located?
 
6. Is the pathology focal, multifocal, or diffuse in its distribution within the nervous system?
 
7. What is the clinical-temporal profile of the neurologic pathology in this patient: acute or chronic; progressive or stable?
 
8. Based upon your answers to the above two questions describe the pathology occurring in this patient.
 
9. If you feel this patient’s pathology is the result of a vascular accident, what vessels are most likely involved?