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A 45-year-old, right-handed, man was brought to the hospital after having a bout of body shaking and loss of consciousness.  He had been previously healthy, but over the past year he had noted a very subtle loss of coordination of his right hand, so that he had difficulty buttoning his shirt, and his handwriting was gradually becoming less neat.  In the past two years, he occasionally had difficulty finding the right words for things.  At first he ignored it, but these problems gradually became more frequent.  The evening of admission, while having dinner with is family, his right hand began to twitch rhythmically.  This was followed by the addition of rhythmic wrist and then elbow flexion.  Next his eyes and face turned upwards and severely toward the right.  After one minute he lost consciousness, fell out of his chair and uttered a brief guttural cry.  This was followed by an assumption of rigid posture with neck and back arched backward.  This posture lasted about one minute.  The jaws were clenched, the mouth foaming, and his breath made a hissing noise though his clenched teeth.  He was incontinent of urine. There was intermittent synchronous jerking of his arms and legs for about three minutes.  The abnormal posture returned briefly, then relaxed, and over the next ten minutes the patient gradually regained consciousness.  He complained of headache, muscle aches in his back, and found his tongue painful, bloody and swollen.  He could remember nothing about what happened to him.

In the Emergency Room, physical exam showed an awake though still lethargic man. He had marked difficulty in expressing himself.  Speech was very slow, missing most adjectives and conjunctions, and generally not very fluent.  His cranial nerve testing was normal except for a marked weakness of the lower right facial muscles.  On the right side of the body there was flaccid paralysis and a Babinski sign.  He could feel pin prick and vibration normally, but light touch, joint position sense and two-point discrimination were impaired on the right side.  Serum glucose, calcium, urea nitrogen and electrolytes were normal.

Twenty-fours hours later, the right-sided paralysis was gone.  He was alert with only minor difficulty naming objects.  There was minimal flattening of the right naso-labial fold and a downward drift of the right arm on extension with eyes closed.  Rapid alternating movements were slowed in the right arm and leg, though strength was normal.  Threshold for sensation of all primary modalities was normal, but he could not name objects placed in his right hand as readily as he could with is left, and two-point discrimination was worse on the right.  The right biceps and triceps reflexes were more active than on the left, but the reflexes in the legs were symmetric, and there was no Babinski sign.

Skull x-rays showed an increased density of bone over the left fronto-parietal area.  The middle meningeal artery grooves were larger and more tortuous on the left side than the right, and on base view, the foramen spinosum was twice was wide on the left side as on the right.  Computerized axial tomography showed an abnormal 3 cm round, flat density over the left fronto-parietal cortex above the Sylvian fissure.  An EEG showed slow waves and spikes over the left fronto-pareital cortex.  On the fourth hospital day, he underwent craniotomy.

QUESTIONS:  CASE SUMMARY 5

1.      What general kind of disease process was going on over the last two years?

2.      What was the episode which prompted hospitalization?

3.      What did the mode of onset of this episode tell you about the location of this pathology?

4.      How does this correlate with the mild symptoms the patient had been experiencing before?

5.      How do you explain the temporary profound weakness and Babinski sign of the day of admission, since he was better the next day?

6.      What is the most common cause if such an occurrence at age 10, 20, 40, 60?

7.      Based on the abnormalities present on skull x-rays, what is the most likely specific pathological diagnosis for the underlying disease?  Why?

8.      Why was it important to determine glucose, calcium, urea nitrogen and electrolytes?

9.      What does the peculiar mature of the sensory disturbance discovered on the second day mean regarding the location of the lesion?

10.  What do spikes mean on an EEG?

11.  If similar attacks continued after appropriate surgical procedure, what would be appropriate therapy?