Path Labs CTools Lab Instructors ImageScope Histology Normals Histology Site M1 Histopathology


Neuropathology Laboratories
Laboratory 2
Diffuse anoxic injury, demyelinating diseases, and infection

Case 2-1
NP009 (H&E)
[WebScope] [ImageScope]

A 44-year-old alcoholic suffered from an episode of acute hemorrhagic pancreatic necrosis with circulatory collapse, renal failure, and respiratory distress. He went into cardiac arrest and was resuscitated after about 10 minutes. Following this he was on a respirator for about one day before being declared deceased. At autopsy there was widespread red mottling of the cerebral cortex grossly. Microscopically, there is widespread neuropil vacuolization of the cortex with only minimal polymorphonuclear leukocytic (neutrophil) infiltration and no appreciable macrophage infiltrates, gliosis, endothelial reactivity, or cavitation. The vessels are congested and have leaked blood and fibrin. The neurons are contracted and eosinophilic (pink/red) with pyknotic (shrunken) nuclei. The glial cells and other cellular elements appear more viable. This same process was also seen in the basal ganglia, and hippocampus, and throughout the rest of the brain.

Diagnosis: Global ischemia

Questions to consider:

  1. What is the overall pathologic process occurring in the brain in this case?
  2. In what regions/cell populations would we expect to see pathologic histologic changes?
  3. What would we expect to see if the patient had survived for 2 weeks?

Case 2-2
NP010A (H&E)
NP010B (Luxol) [WebScope] [ImageScope]
NP010C (Neurofilament) [WebScope] [ImageScope]

A 34-year-old man had various neurologic symptoms for about 8 years, beginning with blurred vision in one eye and followed about 4 years later by diplopia and unsteady gait. Motor difficulties progressed intermittently until severe intention tremors of both upper extremities made it impossible for him to care for himself. He subsequently lost his voice, motor control of his jaw and lower face, and his gag reflex. He could not swallow. His pupils became dilated and fixed. He died about 36 hours after these cranial nerve signs developed. At autopsy, the cerebral white matter showed many sharply demarcated areas of discoloration, particularly in the periventricular areas. Similar lesions were seen in the dorsal part of the portions of the pons, and the caudal region of the floor of the 4th ventricle.

Microscopically, there is extensive rarefaction and loss of myelin in the brainstem areas. There is extensive astrogliosis in the lesions but no significant active inflammation is seen.

Diagnosis: Multiple sclerosis

Questions to consider:

  1. What is the overall pathologic process occurring in the brain in this case?
  2. How do the patient’s symptoms relate to lesion distribution?
  3. What would we expect to see if the patient had come to autopsy early in his disease course?

Case 2-3
NP011A (H&E)
[WebScope] [ImageScope]
NP011B (Luxol) [WebScope] [ImageScope]
NP011C (Neurofilament) [WebScope] [ImageScope]

A 69 year-old male with prior history of coronary heart disease, atrial fibrillation and AML status post bone marrow transplant was admitted to the ED with increasing confusion. The patient’s anticoagulation had recently been discontinued due to thrombocytopenia. A brain MRI showed FLAIR lesions in the parieto-occipital lobe. An MRA of the head and neck showed significant stenosis at the origin of the left internal carotid artery. The patient’s condition progressed relentlessly and he died within one month of his initial presentation. At autopsy, coronal sections of the brain showed multiple irregular, grey and granular areas of softening in the white matter. The larger ones were located at the left superior frontal and superior parietal lobes; however, temporal and occipital lobes and brainstem were also affected.

Microscopically, there are numerous areas of rarefaction and demyelination without significant lymphocytic inflammation. Within the rarefied areas are numerous foamy macrophages, large, bizarre astrocytes, and oligodendroglial cells with glassy intranuclear inclusions.

Diagnosis: Progressive Multifocal Leukoencephalopathy (PML)

Questions to consider:

  1. What is the pathologic process occurring in the brain in this case?
  2. What is the causative organism?

Case 2-4
NP012 (H&E)
[WebScope] [ImageScope]

A 19-year-old student developed chills, headache, nausea, and vomiting. Over the next day, the patient became at first confused and then profoundly obtunded. Physical examination revealed neck rigidity and a petechial skin rash. Although a diagnosis was promptly made, the patient succumbed to his illness. At autopsy, the brain was somewhat edematous and the leptomeninges cloudy. Microscopically, there were a large number of inflammatory cells (predominantly neutrophils) in the leptomeninges. The brain itself is relatively spared by the inflammation. There was a mild degree of edema and a few of the blood vessels near the leptomeninges show minimal inflammation.

Diagnosis: Acute meningitis

Questions to consider:

  1. What is the overall pathologic process occurring in the brain in this case?
  2. What are the most likely causative organisms? What about in neonates? The elderly?
  3. Which CSF abnormalities are usually present in these patients?
  4. What might we expect to observe clinically if the patient had survived?

Case 2-5
NP013 (Trichrome)
[WebScope] [ImageScope]

A 52-year-old alcoholic man sustained a head injury after getting into a fight. He experienced intermittent rhinorrhea for some years thereafter. Approximately 6 weeks before his death, he contracted bronchopneumonia and flu like symptoms. Two weeks later, he was admitted to the ED with confusion and a high fever. A lumbar puncture was performed and CSF showed numerous leukocytes. He was treated for meningitis with antibiotics. Shortly after, he developed hemiparesis and had a convulsion. A brain MRI revealed multiple ring enhancing lesions in the right frontal and temporal regions. An old fracture of the cribriform plate was also recognized and the dural defect overlying it was repaired. A craniotomy was performed; however attempts to drain the lesion were unsuccessful. Two weeks later he died.

At autopsy, there were about 100 cc of blood under the dura over the left hemisphere, hemorrhagic necrosis of the ventral parts of the frontal poles related to the attempts to surgery. There were multiple partially cavitary lesions throughout the forebrain. The largest was in the right mid-temporal region. Similar lesions were seen in the adrenal. Microscopically, the largest lesion exhibited a collagenous wall with a brisk astrocytosis around and within it. The center contained polymorphonuclear leukocytes, cellular debris, and phagocytic macrophages. Much of this has fallen out during sectioning. Some of the macrophages are multinucleate (“foreign body giant cells”).

Diagnosis: Cerebral Abscess

Questions to consider:

  1. What is the differential diagnosis for a ring enhancing lesion in the brain?
  2. What is the pathologic process occurring in the brain in this case?
  3. How did this lesion most likely arise?
  4. How old is this lesion?


Questions or comments? Dr. Killen:

Produced by The Office of Pathology Education
© Copyright 2009 The Regents Of The University Of Michigan. All rights reserved.