Parenchymal Neurosyphilis

Parenchymal neurosyphilis presents 10 to 20 years after the initial infection under several forms.

The characteristic clinical features of tabes dorsalis are summarized in Table 6.6. Grossly, the posterior nerve roots of the spinal cord are thin and grayish, and the posterior columns are translucent and atrophic, chiefly in the lumbosacral segments.

Histologically, the spinal ganglia and the posterior nerve roots show lymphocytic infiltrations, fibrosis, and demyelination. The demyelination proceeds into the posterior columns, which eventually become demyelin-ated throughout the entire length of the spinal cord (Fig. 6.26).

General paresis (dementia paralytica, general paresis of the insane) presents with intellectual decline progressing to severe dementia, mood and personality

FIGURE 6.23

Aspergilloma. A 20-year-old man had a 1-week history of headaches, nausea, somnolence, and left-sided motor and sensory deficits. A. Surgical specimen of an egg-sized aspergilloma resected from the right centroparietal region contains multiple tiny abscesses. B. The microabscesses are separated by granulation tissue composed of fibroblasts, lymphocytes, plasma cells, and multinucleated giant cells. Aspergillus hyphae are apparent at the margin of the abscesses and inside a multinucleated giant cell (PAS stain).

FIGURE 6.24

Cerebral candidiasis. A and B. Multiple microabscesses in the cortex and white matter (HE).

FIGURE 6.24

Cerebral candidiasis. A and B. Multiple microabscesses in the cortex and white matter (HE).

FIGURE 6.25

Meningovascular syphilis. A. Massive subarachnoid exudate with lymphocytes and plasma cells. B. Mural thickening and luminal reduction of a parenchymal artery (HE).

FIGURE 6.26

Tabes dorsalis. A. Macrosection of lumbar spinal cord section showing demyelination of the posterior nerve roots and posterior columns. B. Higherpower view of the demyelinated posterior nerve roots and the normal anterior nerve roots (iron hematoxylin-picrofuchsin stain).

FIGURE 6.26

Tabes dorsalis. A. Macrosection of lumbar spinal cord section showing demyelination of the posterior nerve roots and posterior columns. B. Higherpower view of the demyelinated posterior nerve roots and the normal anterior nerve roots (iron hematoxylin-picrofuchsin stain).

changes, grandiose delusions, inappropriate joking, and disregard for social standards. Dysarthric speech, impaired visual acuity, pupillary changes, tremor, ataxia, myoclonic jerks, and seizures may develop any time during the course of the disease.

Grossly, the brain volume is reduced. The leptomen-inges are thick, mostly over the frontal lobes, which are severely atrophic. On sections, the ventricles are dilated and the ependyma is finely granular (granular ependymitis).

Histologically, general paresis is a syphilitic menin-goencephalitis. Lymphocytic and plasma cell perivascu-lar infiltrations are prominent in the leptomeninges, cerebral cortex, white matter, and deep gray structures. Hypertrophied, rod-shaped activated microglial cells diffusely infiltrate the cerebral cortex. Neuronal losses are widespread and particularly severe in the frontal lobes. Astrocytosis is usually proportional to the neuronal losses. In untreated cases, the spirochetes are demonstrable with silver stain (Fig. 6.27).

In syphilitic optic atrophy, a progressive loss of visual acuity may occur alone or may complicate tabes dorsalis and general paresis. The nerves show lympho-cytic infiltrations, fibrosis, and degeneration of myelin.

Gumma or syphilitic granuloma, a very rare form of infection, presents as a firm mass in the meninges or brain parenchyma. Histologically, it contains areas of coagulation necrosis surrounded by epithelioid cells,

TABLE 6.6

Clinical Presentations of Tabes Dorsalis

Symptoms

Lightning-lancinating pain in legs Paresthesias in extremities

Visceral crisis; sharp pain of sudden onset, variable duration. and abrupt end

Signs

Argyll-Robertson pupils: small, irregular unequal pupils, do not constrict to light, constrict on accommodation Optic atrophy

Absent knee and ankle reflexes

Loss of vibratory and position sensations

Variable loss of touch, pain, and thermal sensations

Romberg sign: positive

Gait: sensory ataxic

Autonomic dysfunction: urinary overflow, incontinence

(insensitive atonic bladder), constipation, impotence Trophic changes: perforating ulcers in feet Charcot joints: insensitive arthropathy

Neurosyphilis

FIGURE 6.27

General paresis A. Chronic fibrotic leptomeningitis over the frontal lobe (HE). B. Perivascular infiltration with lymphocytes and plasma cells in the subarachnoid space and parenchyma (Cresyl-violet). C and D. Hypertrophied, rod-shaped microglia in the cerebral cortex (Cresyl-violet and Hortega silver stain). E. Ependymitis granulosa in the ventricular wall (HE). F. Colonies of spirochetes in an untreated case (silver stain).

FIGURE 6.27

General paresis A. Chronic fibrotic leptomeningitis over the frontal lobe (HE). B. Perivascular infiltration with lymphocytes and plasma cells in the subarachnoid space and parenchyma (Cresyl-violet). C and D. Hypertrophied, rod-shaped microglia in the cerebral cortex (Cresyl-violet and Hortega silver stain). E. Ependymitis granulosa in the ventricular wall (HE). F. Colonies of spirochetes in an untreated case (silver stain).

lymphoplasmacytic infiltrations, fibroblasts, and occasional giant cells.

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