Alcohol Associated Pathology

Slide 55 & Slide 56

The section depicted in slide 55 is pretty much diagnostic. The critical finding is atrophy of ?. Click here.

If you noted the anterior lobe of the cerebellar vermis, in your Wernicke’s list you were correct. Slide 56 depicts the typical narrowing of folia and widening of sulci seen grossly in cortical atrophy, be it cerebellar, as in this instance, or cerebral. What clinical phenomena relate to this finding? To what extent do you think peripheral neuropathy, a common occurrence in alcoholism, contributes to ataxia? Malnutrition is an important etiological factor in the pathology of Wernicke’s disease. One of Wernicke’s cases was a non alcoholic pregnant woman with uncontrolled prolonged vomiting.

Slide 57

Slide 57 shows an uncommon lesion, central pontine myelinolysis. This myelinolytic process appears to be produced by too rapid corrections of electrolyte abnormalities. The latter are the consequence of GI fluid loss.

Trauma and Cerebral Herniation

Slide 58 & Slide 59

Slide 58 shows the dura pulled back over a swollen hemisphere. Note the subdural blood clot. This patient had slowly expanding bilaterral subdural hematoma. In older people or those with bleeding tendencies, the inciting head trauma may be inapparent. The associated change in mental status was unfortunately not recognized, perhaps because he was a chronically hospitalized psychiatric patient. Nothing like being under constant medical observation! The process produced elevated intracranial pressure, bi- hemispheric compression and bilateral transtentorial herniation of the medial temporal lobes (unci). These consequences can be seen in slides 59, of this patient, and 60 (below), from another case.

Pictures 60-63 illustrate transtentorial uncal herniation and the secondary effects of such herniation in the rostral brain stem and occipital lobes . Note in 60 and 61( at higher magnification) the sharp groving of each uncus. This photograph, of the base of the brain, illustrates the proximity of the 3^rd cranial nerve to the herniating unci. Other vulnerable structures, not well shown here, are the posterior cerebral arteries. Should the patient survive, compression of these can lead to necrosis of the visual cortex and blindness. Jump over to slide 63 which illustrates bilateral occipital lobe hemorrhagic infarctions..

An important consequence of uncal herniation is illustrated in slide 62 which depicts necrosis and secondary brain stem hemorrhages in the rostral pons. Mid-brain and rostral pons are compressed and distorted by the process of transtentorial uncal herniation

Slide 60 & Slide 61

Slide 62 & Slide 63

Slide 64 (below) depicts unilateral uncal herniation due to a supra tentorial mass lesion on the same side. This picture very graffically presents necrosis of the herniating uncus and compression with displacement of the midbrain. When the pressure rises in the posterior fossa, a similar event occurs. This may be the consequence of herniation from above the tentorium, central herniation, or from a mass lesion within the posterior fossa. In such cases what herniates? Where? Compressing what? If you answered: cerebellar tonsils, foramen magnum, medulla you were correct.

Slide 64