Objective: To describe some clinical features of movement disorders after cerebral anoxia.

Background: The basal ganglia, especially the globi pallidi (GP), are highly vulnerable to generalized cerebral anoxia hypoxia. Cerebral hypoxia ischemia typically produces lesions of the globus pallidus and striatum that may result in not only an akinetic rigid syndrome but also in other movement disorders, including dystonia, chorea, tics, athetosis, tremor, and myoclonus

Methods: We report on 3 cases with a parkinsonism, dystonia and myoclonus secondary to hypoxic-anoxic encephalopathy

Results: Case-1 A 34-year-old woman developed a sudden cardiac arrest after a hysterectomy due to severe hemorrhage. She remained in coma for 10 days, followed by a gradual increase in her level of consciousness. She was noted to be normal intellectual, severely rigid and akinetic and had rest and kinetic tremor at this time. Speech was monotonous, ataxic and dysarthric limited to articulate. She was unable to stand and walk without support.  Head MRI scan after 1 month showed bilateral low densities in the globus pallidus  and more putamen. Treatment with clonazepam, trihexyphenidyl and levodopa/carbidopa resulted in a mild improvement. Examination 1 month later revealed that her speech, gait, tremor were improved but still had marked postural instability.  Case-2. A 41-year-old woman suffered an acute asthmatic attack followed by cardiorespiratory arrest. She gradually regained consciousness over several weeks. Neurological examination revealed severe dystonic posturing of all her limbs and walking was unable.  CT scan of the head showed bilateral symmetrical hypo densities globus pallidus. Treatment with trihexyphenidyl and levodopa/carbidopa resulted in a moderate improvement. Examination 1 year later  revealed marked dystonic rigidity of her limbs. Case-3. A 19-year-man developed a sudden cardiac arrest during a surgery for pulmonary tuberculosis haemorrhage. He remained in coma for 2-3 weeks, followed by several seizures with a good response to antiepileptic drugs (AED). Examination was revealed mild cognitive impairment, severe dysarhria, and mild spastic paresis of his limbs. He was in bed and unable to walk. Head MRI scan showed cortical laminar necrosis. Spike-and-wave discharges were recorded in the EEG. Treatment with AED including valproic acid (VPA), livetyracetam and clonazepam and rehabilitation resulted in a marked improvement. Examination 11 months later revealed that his intellect and speech were much improved. He noticed involuntary “shaking” movements of his limbs more on the legs while walking. His gait was slight ataxic and difficulties in tandem gait.

Conclusions: All three of our cases suffered hypoxic-ischemic insults to the brain; however, the clinical outcomes and MRI and CT scans were dissimilar. Diversity of clinical features may be depending on different neuropathological damage and neurotransmitter disbalance within the basal ganglia after a hypoxic-ischemic arrest, as seen in our patients, further emphasizes the need for advances in therapy.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/some-clincal-features-of-movement-disorders-after-cerebral-anoxia/