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[A case report of infarction of the bilateral thalamus and the midbrain]
Abstract:
A 63 years old man was admitted because of coma of 24 hours duration. He had a history of infarction of the medulla oblongata 7 months earlier. On admission he was unconscious and had right oculomotor nerve palsy. To a painful stimulus, he responded with only a slight body movement. On the CT scan, low density areas were seen in the bilateral thalamus and the midbrain. In the next day he recovered from coma and abnormal behaviors appeared such as wondering in the ward, touching other patient's face and manipulating his stool. Verbal expression was extremely poor. Chlorpromazine was needed to suppress abnormal behaviors. Thereafter, abnormal behaviors gradually subsided and by the 23 hospital day he became bedridden even when chlorpromazine was withdrawn. At that time, he said only "yes" or "no" in response to questions and only few spontaneous movements were observed. From the 40 hospital day he suffered from pneumonia and gradually sank into the state of akinetic mutism. He died on the 50 hospital day. Pathologically, infarctions destroyed the n. parafascicularis, n. centromedianus and the intralaminar nuclei in the left thalamus, n. parafascicularis and a part of n. centromedianus in the right. In the medulla oblongata, right n. ambiguous and reticular formation were destroyed. Both thalamic lesions extended posteriorly to unite with the midbrain lesion.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
A patient with a history of brainstem stroke developed coma and abnormal behaviors following bilateral thalamic and midbrain infarctions. Neuropathology revealed extensive lesions, leading to akinetic mutism and death.
Area of Science:
- Neurology
- Neuroscience
- Pathology
Background:
- The case presents a 63-year-old male with a prior history of medulla oblongata infarction.
- The patient was admitted due to a 24-hour coma and right oculomotor nerve palsy.
Observation:
- Initial CT scans revealed low-density areas in the bilateral thalamus and midbrain.
- Following recovery from coma, the patient exhibited abnormal behaviors including wandering and poor verbal expression, requiring chlorpromazine.
- The patient's condition progressed to akinetic mutism, pneumonia, and ultimately death.
Findings:
- Pathological examination confirmed infarctions in the thalamus (bilateral parafascicular, centromedianus nuclei, intralaminar nuclei) and midbrain.
- Lesions in the medulla oblongata included the right nucleus ambiguous and reticular formation.
- Thalamic lesions extended to the midbrain, indicating widespread brainstem and diencephalic damage.
Implications:
- This case highlights the severe neurological deficits, including behavioral changes and akinetic mutism, that can result from extensive thalamic and midbrain infarctions.
- The findings underscore the critical role of the thalamus and midbrain in maintaining consciousness, behavior, and motor function.
- Understanding these lesion-behavior correlations is crucial for diagnosing and managing patients with complex brainstem and diencephalic injuries.