Poliomyelitis

Abstract

THROUGHOUT the literature there are numerous references to the involvement of the cerebellum in poliomyelitis; still clinical evidence of disturbances of this region of the nervous system is generally lacking. This may be due to the fact that it is somewhat difficult and unsatisfactory to examine cerebellar function in patients severely paralyzed with spinal poliomyelitis or critically ill with bulbar or respiratory poliomyelitis. Certainly, in most studies evidence of residual cerebellar disturbances in patients that have recovered from this illness is generally lacking. Because of the volume of our material it was felt that a detailed study of the cerebellum might be of value in indicating the actual nature and extent of the cerebellar lesions in this disease.As early as 1898 M\l=e'\din 1 reported cases of poliomyelitis in which the chief finding was incoordination. He referred to these cases as the ataxic, or cerebellar, form of the disease. He described these patients as having an uncertain, staggering, and wide-based gait, similar to patients with Friedreich's ataxia. Wickman 2 also reported cases in which ataxic symptoms were conspicuous and were associated in many cases with diminution or loss of tendon reflexes. Occasionally the cerebellar disturbances were mild and often hidden by the other, more classical findings of the disease. In a pathologic study of four cases, Wickman observed fairly intense changes in the cerebellum in three. These consisted of perivascular infiltrationsinvolving both the cortex and the white matter primarily of the vermis. The meninges surrounding the cerebellum also showed mild scattered areas of mononuclears.Ataxia has frequently been mentioned in subsequent epidemics by Zappert,3 Lindner and Mally,4 Lemmon,0 Horányi-Hechst," and Fanconi and associates.7 Horányi-Hechst, in a study of 38 fatal cases, observed cerebellar changes in 22, or 58%. Fanconi and his associates described cerebellar changes in only 3.2% of their 375 cases. Lemmon reviewed in detail the clinical symptoms and signs in 49 patients with acute poliomyelitis and found only one case that clinically represented cerebellar poliomyelitis. The symptoms in this case consisted of extreme lateral nystagmus, vertigo, intention tremor, and ataxia.There is a great diversity of opinion in the literature regarding the distribution of the lesions within the cerebellum in poliomyelitis. Generally most investigators feel that the Purkinje cells are spared and that most of the lesions are limited to the

Cerebellar remodelling decades after spinal cord insult: neuroplasticity in poliomyelitis survivors

“…Our study provides compelling in vivo evidence of cerebellar changes in adult poliomyelitis survivors with reference to healthy controls. In contrast to previous postmortem studies [9,14,15] and sporadic clinical reports [16][17][18], the cohort of adult poliomyelitis survivors evaluated in this study did not exhibit cerebellar atrophy. On the contrary, polio survivors exhibited hypertrophic changes in the cerebellum.…”

“…Reports of cortical involvement are inconsistent; it is thought to be limited to motor and pre-motor areas [9] and the cerebellar pathology limited to the vermis and deep cerebellar nuclei. Accounts of involvement of cerebellar cortical layers are strikingly conflicting [9,10,14,15]. Sporadic cerebellar manifestations, such as ataxia, nystagmus, vertigo and intention tremor had been linked to poliovirus type 1 [16][17][18].…”

“…Sporadic cerebellar manifestations, such as ataxia, nystagmus, vertigo and intention tremor had been linked to poliovirus type 1 [16][17][18]. The rarity of frank cerebellar findings was hypothesised to be due to limited cerebellar degeneration and the challenge of ascertaining cerebellar signs in the presence of widespread lower motor neuron degeneration [15]. More recent functional [19,20] and structural [21] studies speculate that supraspinal alterations may represent adaptive processes in response to longstanding lower motor neuron loss.…”