Pure Motor Hemiplegia due to Meningovascular Neurosyphilis

Johns, Donald R.; Tierney, Maureen; Parker, Stephen W.

doi:10.1001/archneur.1987.00520220060018

Cited by 34 publications

(11 citation statements)

References 22 publications

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“…213 The important idea is that the neurologic deficit (syndrome) depends on the size and site of the lesion and that there can be an infinite number of "lacunar syndromes." The site of the lesion does not precisely determine its pathogenesis as infarction, hemorrhage, infection, 23 or neoplasm. 24 CT has established that small intracerebral hemorrhages 25 - 26 and large ischemic infarcts 27 can cause "lacunar syndromes."…”

mentioning

confidence: 99%

The fallacy of the lacune hypothesis.

Millikan

Futrell

1990

Stroke

153

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We review the definition, pathogenesis, natural history, and prognosis and describe the first experimental model of lacunes. Defined pathologically or radiologically, lacunes are small cerebral infarcts which become cystic and are caused by occlusion of small arteries. The clinical definition of lacune is confused. The word "lacune" means a small stroke. While the immediate mortality rate from a small stroke is low, many patients are unable to return to work and the long-term prognosis is guarded. Photochemical damage to the carotid artery of rats produces microemboli to the brain, resulting in cavitary lesions resembling lacunes in humans. The "lacune hypothesis" is a fallacy because small cerebral infarcts are not caused solely by a combination of hypertension and small vessel disease, and the various "lacunar syndromes" are simply small strokes which should be investigated as such. (Stroke 1990;21:1251-1257) T he "lacune hypothesis" states that lacunes are caused by a combination of hypertension and characteristic vascular lesions involving single perforating brain arteries.

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mentioning

confidence: 99%

The fallacy of the lacune hypothesis.

Millikan

Futrell

1990

Stroke

153

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“…There is excessive fibrotic tissue in the adventitia with lymphocytic and plasma cell infiltration. All these changes are conditions for luminal narrowing that can lead to arterial thrombosis with the subsequent development of an infarction [15,16]. In Nissl-Alzheimcr's arteritis, arteritis of small intracranial vessels is dem onstrated, and may also cause vascular occlusion [10,16], The meningeal and vascular types of neurosyphilis are explained by the inflammatory pro cesses of 'endarteritis obliterans', Heubner's and NisslAlzheimer's arteritis.…”

Section: Syphilismentioning

confidence: 99%

“…When the inflamm ation is focal, it is charac terized by the appearance o f luetic hemiplegia, associated with other signs such as altered mental status, disartria, aphasia or positive frontal release signs [9], whereas when there is multifocal involvement of small intracranial ar teries by syphilitic vasculitis, the clinical picture is one of a slow but progressive loss of cognitive functioning and personality changes and has to be differentiated from other vascular dementias, such as 'etat lacunaire', Binswanger or multi-infarct dementias [13]. More rarely, meningovascular syphilis may present as a lacunar stroke syndrome, manifested by: hemiataxia-hypesthesia due to arteritis of the perforating branches to the lateral thala mus [24]; hemiparesis-ataxia with m otor deficits and cer ebellar disfunction [25], or pure m otor hemiplegia [15]. Meningovascular syphilis may even present as a dorsal m idbrain syndrome with cognitive dysfunction [26].…”

Section: Clinical Featuresmentioning

confidence: 99%

“…40] were the first authors to describe the accelerated develop ment of ncurosyphilis in HIV-infected patients; since that description, it has been suggested that coinfection with HIV alters the course of T. pallidum infection and its response to treatm ent. However, other evidence suggests that severe neurosvphilis cases in HIV-infected patients may be the exception, not the rule, and that syphilis pre sentation usually does not differ even when there is a posi tive HIV serologic status [2,15,17], There are several possible mechanisms of pathogenic interaction between HIV and T. pallidum. O f paramount importance is the possibility that the immunodeficiency state induced by HIV may reduce the immunological response to treponemal infection via the profound im pairm ent of cell-mediated immunity and the functional defects of macrophage function created by this state, impairing the host defense against syphilis and facilitating its progression [6,15,28,[40][41][42].…”

Section: N Eurosyp Hilis In Hiv-infected Patientsmentioning

confidence: 99%

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Cerebrovascular Complications of Neurosyphilis: The Return of an Old Problem

et al. 1996

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Neurosyphilis is increasing due to a rise in the number of cases of syphilis in cocaine/crack addicts and in patients with HIV infection. Neurosyphilis is an example of a unique group of chronic CNS diseases that may cause either a degenerative or a vasculitic process, where the main pathogenic event is ''endarteritis obliterans'' of terminal arterioles. In meningovascular neurosyphilis, the most commonly involved artery is the middle cerebral artery. It generally presents with a prodromic phase, weeks or months before the onset of identifiable vascular syndromes. When there is focal inflammation the clinical picture is characterized by hemiplegia, whereas in the case of multifocal involvement of small intracranial arteries, it presents with a slowly progressive loss of cognitive functioning and personality changes. Since neurological deficits once established may only slightly improve with treatment, the goal of therapy is to halt the progression of the disease. Intravenous aqueous crystallin penicillin G is the most accepted treatment. HIV-infected patients have shown accelerated development of neurosyphilis, and it is suggested that coinfection with HIV alters the course of Treponema pallidum infection. Atypical manifestations of neurosyphilis have been reported among HIV patients, including fulminant presentation, rapid progression, atypical serological findings, and failure of conventional doses of penicillin to eradicate infection.

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“…11 Parasitic diseases of the central nervous system could also cause PMH, but they have not been described in this setting. We report a patient with cysticercosis and PMH.…”

Section: Neurocysticercosis and Purementioning

confidence: 99%

Neurocysticercosis and pure motor hemiparesis.

Barinagarrementería

Brutto

1988

Stroke

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A 49-year-old man with meningeal cysticercosis presented with a pure motor hemiparesis. Computed tomography and magnetic resonance imaging showed a capsular infarction and a suprasellar cyst with surrounding arachnoiditis. Cerebrospinal fluid analysis confirmed the diagnosis as it showed positive immunologic reactions to cysticerci. This is the first reported case of pure motor hemiparesis due to a parasitic disease of the central nervous system. (Stroke

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Pure Motor Hemiplegia due to Meningovascular Neurosyphilis

Cited by 34 publications

References 22 publications

The fallacy of the lacune hypothesis.

The fallacy of the lacune hypothesis.

Cerebrovascular Complications of Neurosyphilis: The Return of an Old Problem

Neurocysticercosis and pure motor hemiparesis.

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