Date: Sunday, October 7, 2018
Session Title: Parkinsonism, MSA, PSP (Secondary and Parkinsonism-Plus)
Session Time: 1:45pm-3:15pm
Location: Hall 3FG
Objective: To present a case of parkinsonism due to the hypoxic-ischemic lesions of the striatum.
Background: Parkinsonism due to the basal ganglia lesions caused by hypoxic-ischemic brain injury is rarely reported. It is most commonly caused by lesions of the lenticular nucleus and parkinsonism due to the striatal lesions has been rarely reported.
Methods: A-44-year old female with a 15 year history of temporal lobe epilepsy had cardiac arrest due to the recurrent secondary generalized epileptic seizures. She received cardio-pulmonary resuscitation for 10 minutes and then received assisted ventilation for 6 days in intensive care unit. She was taking oxcarbazepine (1200 mg/day) and lamotrigine (200 mg/day) as antiepileptic treatment. At the end of 6 days, assisted ventilation was ended and patient was extubated.
Results: She was conscious and neurological examination additionally revealed bradimimia, hypophonia, symmetric bradikinesia and rigidity (lead pipe). Myoclonus and rest tremor were not seen on examination. Brain magnetic resonance imaging showed bilateral hyper intense ischemic lesions at striatum in T2W and FLAIR images, and generalized slow wave activity with theta frequency was seen in electroencephalography. Levodopa treatment (levodopa/benserazide 100/25 mg, three times a day) was initiated for parkinsonism. In the following weeks, moderate improvement of bradikinesia and rigidity was seen after initiation of levodopa treatment. Parkinsonism was thought to be due to the hypoxic-ischemic lesions of the striatum.
Conclusions: Movement disorders, especially myoclonus, can be seen in patients following hypoxic-ischemic brain injury. Although the basal ganglia are thought to be vulnerable to hypoxia, parkinsonism following hypoxic-ischemic brain injury is not common and akinetic-rigid parkinsonism due to the striatal lesions has been rarely reported. The underlying pathophysiology is thought to result from inadequate disinhibition of thalamic projections of the motor cortices due to the hypoxic-ischemic damage of basal ganglia. The clinical syndrome corresponds to postsynaptic loss of striatal D2 receptor efficiency. Improvement with levodopa may be related to the amount of postsynaptic striatal D2-receptor loss.
To cite this abstract in AMA style:H. Kaleagasi, N. Oksuz, O. Dogu. A Case of Parkinsonism due to the Hypoxic-Ischemic Lesions of the Striatum [abstract]. Mov Disord. 2018; 33 (suppl 2). https://www.mdsabstracts.org/abstract/a-case-of-parkinsonism-due-to-the-hypoxic-ischemic-lesions-of-the-striatum/. Accessed December 10, 2023.
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