Slide 158
Questions:
1. What do the clinical findings indicate? Meningitis should be considered in any patient with fever and mental or neurologic symptoms. The most immediate clinical effects of acute subarachnoid suppuration, distinguishing it from infections in other parts of the body, are severe headache, generalized convulsions, and a disorder of consciousness (i.e., drowsiness, stupor, or coma). The clinical sign of stiffness of the neck (resistance to passive movement) on forward bending is an important sign of inflamed piarachnoid. Kernig and Brudzinski's signs, extension of neck and flexion of hips and knees, reduce stretch on inflamed spinal structures.
Toxic effect of the brain tissue beneath the pia leads to symptoms of confusion, stupor, coma and convulsions.
2. What laboratory tests would have been useful in evaluating this patient?
Cerebrospinal fluid evaluation of sugar, protein and white blood cell count:
1. Low sugar, high protein and high white count (>1000/mm) generally indicate bacterial infection.
2. Normal sugar, modestly increased protein and fewer than 1000 WBC/mm indicates viral etiology
3. Low sugar, high protein and slight increase in WBC indicates fungal infections and chronic bacterial infections.
3. What parts of the central nervous system may be involved with purulent bacterial infections?
A. Meningeal
1) Leptomeningitis
2) Subdural empyema
3) Epidural abscess
B. Parencymatous-brain abscess
Slide 170
Questions:
1. What are the histologic features that differentiate this lesion from a contusion?
Contusions occur at the crest of gyri, while ischemic insults are almost invariably more severe within the depths of sulci. The molecular layer of the cortex, which is regularly spared in an infarct, is often disrupted in contusions. This lesion involves the base of the sulci and the molecular layer is spared indicating the lesion is ischemic and not a contusion.
2. What does laminar necrosis of the cerebral cortex mean?
Laminar necrosis is a type of cortical necrosis in which the pyramidal cell layer of the cortex is more severely affected than the granular layers.
3. What factors may contribute to cerebral infarction?
A. Chief causes are thrombosis superimposed on atherosclerosis and embolus.
B. Other factors contributing to infarction include:
1) decreased oxygenation of the blood from reduced hemoglobin, or hypoxemia
2) decreased perfusion from cardiac arrest, hypotension, shock, pulmonary embolism, or venous stasis (CHF, increased intracranial pressure)
3) altered composition of blood (polycythemia, TTP, pregnancy, etc)
4) other factors: hypoglycemia vasculitis, infection with local thrombosis or endarteitis obliterans, or compression of vessels by tumor, aneurysm, steal syndromes etc.
4. How does the site of occlusion and the rapidity of occlusion effect the extent of infarction?
The more proximal the occlusion, the more extensive the infarct.
The more rapid the occlusion, the more extensive the infarct.
(Collateral circulation via ophthalmic artery, circle of Willis and leptomeningeal anastomoses affect extent)