[Post-traumatic focal dystonia after contralateral thalamic lesion]. / Posttraumatische fokale Dystonie nach kontralateraler Thalamusläsion.

Dystonia rarely is a consequence of head trauma. In most of these patients lesions of the contralateral caudate or putamen are found. We report a 27-year-old patient who displayed focal dystonia of the right hand with the latency of four months after he had sustained a severe head trauma. The development of a lesion in the contralateral dorsolateral thalamus within the first weeks after the craniocerebral injury is demonstrated with sequential computertomographic and magnetic resonance imaging. There were no lesions of the caudate or the putamen.

Posttraumatic movement disorders after moderate or mild head injury.

We examined the occurrence of posttraumatic movement disorders after moderate or mild head injury with a three-level follow-up study including questionnaires, telephone interviews, and personal examinations 4-6 years after the trauma (mean 5.2 years). Sixteen of 158 patients (10.1%) for whom a detailed follow-up was available had developed movement disorders most probably related to craniocerebral trauma. The most frequent finding was a low-amplitude postural/intention tremor that appeared to resemble enhanced physiological or essential tremor. Twelve patients reported transient tremor, two patients had persistent tremor, one patient had transient tremor and persistent hyperekplexia, and another patient had mild persistent cervical myoclonic twitches. Overall, the movement disorder was transient in 12 patients (7.6%) and persisted in only 4 patients (2.6%). These movement disorders were not disabling and did not require medical therapy. Taking into account possible bias by selection of the sample group, the frequency of movement disorders secondary to moderate or mild head trauma might be lower than 10.1%. Posttraumatic movement disorders occurred significantly more often in the group of patients with Glasgow Coma Scores between 9 and 14 than in those with a score of 15. Severe movement disorders such as low-frequency kinetic tremor or hemidystonia were not identified in this survey.

Tremor and dystonia after penetrating diencephalic-mesencephalic trauma.

Isolated post-traumatic basal ganglia or brainstem lesions secondary to direct injury resulting in movement disorders, such as tremor or dystonia, are extremely rare. We report an unusual case with a 4-5 Hz rest and postural tremor and focal action-induced dystonia of the left arm. The movement disorder developed within 2 years of the patient sustaining a right-sided mesencephalic-diencephalic lesion due to a penetrating thrust injury with a screwdriver. Magnetic resonance imaging demonstrated involvement of the cerebral peduncle, the substantia nigra, the subthalamic region and the thalamus.

Post-traumatic movement disorders in survivors of severe head injury.

The present study investigates the occurrence of post-traumatic movement disorders in survivors of severe head injury. We studied a series of 398 consecutive patients who were admitted to the hospital with a Glasgow Coma Score of 8 or less after they sustained a head trauma. One hundred thirty-four out of 398 patients (34%) died after they were admitted to the hospital or in the further course. A recent follow-up was obtained in 221 of the 264 remaining patients (84%). Follow-up consisted of a three-level assessment, including questionnaires, telephone interviews, and personal examinations. Fifty out of 221 patients (22.6%) had developed movement disorders secondary to the head trauma, which were transient in 23 patients (10.4%) and persistent in 27 patients (12.2%). Forty-two patients (19%) had tremors, nine (4.1%) had dystonia, and seven (3.2%) had other movement disorders. Twelve patients (5.4%) had disabling low-frequency kinetic tremors (2.5 to 4 Hz) or dystonia, or both. Low-frequency kinetic tremors developed with a latency from 2 weeks to 6 months after trauma, and dystonia with a latency from 2 months to 2 years. When compared with patients without movement disorders, this subgroup was characterized by a different distribution profile of Glasgow Coma Scores with a higher proportion of lower scores on admission (p < 0.05). When we compared the initial CT findings, there were highly significant associations between generalized brain edema and the occurrence of any movement disorders, between generalized brain edema and the occurrence of persistent movement disorders, and between generalized brain edema and the occurrence of kinetic tremors and dystonia. We detected similar associations for focal cerebral lesions, but not for subdural and epidural hematomas. In conclusion, transient or persistent movement disorders are common sequelae in survivors of severe head injury. Disabling movement disorders such as kinetic tremors and dystonia, however, occur only in a small group of patients.

Lesion of dentatothalamic pathways in severe post-traumatic tremor.

The present study investigates evidence of dentatothalamic pathway lesions in nineteen patients with severe kinetic post-traumatic tremor respectively by magnetic resonance imaging (MRI). Kinetic tremor is thought to be characteristic of lesions of the cerebellar outflow. While this hypothesis is supported by experimental data, neuropathological and neuroradiological findings have been limited. The appendicular tremors were unilateral in 13 patients and bilateral in 6, accounting for 25 instances of tremor. The tremor developed after severe head trauma in 18 patients. These patients had evidence of diffuse axonal injury on MRI. Postural and kinetic tremor was present in all patients, and was accompanied by tremor also present at rest in 14 instances. Multiplanar MRI studies were performed on a high-field MRI system operating at 2.0 T in 13 patients and on intermediate-field strength MRI systems in 6 patients according to a standardized protocol. To detect small deposits of hemosiderin after post-traumatic lesions, the protocol included a heavily T2-weighted spin-echo pulse sequence. Lesions of the dentatothalamic pathways were found in 22 instances. The lesions were classified into different types of according to their distribution. A lesion of the dentate nucleus ipsilateral to the tremor (type 1) was found in one instance (4%), lesions involving the ipsilateral predecussational dentatothalamic pathway (type II and III) were found in 14 instances (56%), and lesions involving the contralateral post-decussational course (type IV) in 7 instances (28%). One patient with a mild head trauma had a lesion of the contralateral thalamus. The lesions appeared as hypointense, hyperintense or mixed. Two of three patients with a parkinsonian-like rest tremor had type IV lesions involving the substantia nigra. The nosological concepts of tremors are discussed. 'Midbrain' tremor may have distinct pathoanatomical lesion sites.