Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: A clinicopathological case study
Identifieur interne : 000642 ( PascalFrancis/Curation ); précédent : 000641; suivant : 000643Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: A clinicopathological case study
Auteurs : José Berciano [Espagne] ; Francesc Valldeoriola [Espagne] ; Isidre Ferrer [Espagne] ; Jordi Rumia [Espagne] ; Julio Pascual [Espagne] ; Concepcion Marin [Espagne] ; Maria J. Rey [Espagne] ; Eduardo Tolosa [Espagne]Source :
- Movement disorders [ 0885-3185 ] ; 2002.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Personne âgée.
English descriptors
- KwdEn :
Abstract
We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa-responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation.
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<front><div type="abstract" xml:lang="en">We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa-responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation.</div>
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<s5>46</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>47</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>47</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>47</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>49</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>49</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>49</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Trouble neurologique</s0>
<s5>53</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Neurological disorder</s0>
<s5>53</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>53</s5>
</fC07>
<fN21><s1>266</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>
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