Passive accessory joint mobilization in the multimodal management of chronic dysesthesia following thalamic stroke.

Study design: Case Report. Purpose: Stroke is the most common cause of long-term disability. Dysesthesia, an unpleasant sensory disturbance, is common following thalamic stroke and evidence-based interventions for this impairment are limited. The purpose of this case report was to describe a decrease in dysesthesia following manual therapy intervention in a patient with history of right lacunar thalamic stroke. Case description: A 66-year-old female presented with tingling and dysesthesia in left hemisensory distribution including left trunk and upper/lower extremities, limiting function. Decreased left shoulder active range of motion, positive sensory symptoms but no sensory loss in light touch was found. She denied pain and moderate shoulder muscular weakness was demonstrated. Laterality testing revealed right/left limb discrimination deficits and neglect-like symptoms were reported. Passive accessory joint motion assessment of glenohumeral and thoracic spine revealed hypomobility and provoked dysesthesia. Interventions included passive oscillatory joint mobilization of glenohumeral joint, thoracic spine, ribs and shoulder strengthening. Results: After six sessions, shoulder function, active range of motion, strength improved and dysesthesia decreased. Global Rating of Change Scale was +5 and QuickDASH score decreased from 45% to 22% disability. Laterality testing was unchanged. Conclusion: Manual therapy may be a beneficial intervention in management of thalamic stroke-related dysesthesia. Implications for Rehabilitation While pain is common following thalamic stroke, patients may present with chronic paresthesia or dysesthesia, often in a hemisensory distribution. Passive movement may promote inhibition of hyperexcitable cortical pathways, which may diminish aberrant sensations. Passive oscillatory manual therapy may be an effective way to treat sensory disturbances such as paresthesias or dysesthesia.

Aphasia and unilateral spatial neglect due to acute thalamic hemorrhage: clinical correlations and outcomes.

Thalamic hemorrhages are associated with a variety of cognitive dysfunctions, and it is well known that such cognitive changes constitute a limiting factor of recovery of the activities of daily living (ADL). The relationship between cognitive dysfunction and hematomas is unclear. In this study, we investigated the relationship between aphasia/neglect and hematoma volume, hematoma type, and the ADL. One hundred fifteen patients with thalamic hemorrhage (70 men and 45 women) were studied. Their mean age was 68.9 ± 10.3 years, and patients with both left and right lesions were included. We calculated hematoma volume and examined the presence or absence of aphasia/neglect and the relationships between these dysfunctions and hematoma volume, hematoma type, and the ADL. Fifty-nine patients were found to have aphasia and 35 were found to have neglect. Although there was no relationship between hematoma type and cognitive dysfunction, hematoma volume showed a correlation with the severity of cognitive dysfunction. The ADL score and ratio of patient discharge for patients with aphasia/neglect were lower than those for patients without aphasia/neglect. We observed a correlation between the hematoma volume in thalamic hemorrhage and cognitive dysfunction. Aphasia/neglect is found frequently in patients with acute thalamic hemorrhage and may influence the ADL.

Stuttering after right cerebellar infarction: a case study.

UNLABELLED: We report a male patient with neurogenic stuttering after cerebellar infarction. He had suffered from frontal and thalamus damage and he had exhibited aphasia, but his speech had been fluent until onset of the cerebellar infarction. Results of analysis of speech samples included the following: (1) the patient showed very frequent syllable repetition and part-word repetition. (2) The stuttering occurrence rate at the second test was much higher than at the first test. (3) Almost all stuttering occurred on initial word sounds; stuttering on the medial and final word was less frequent. (4) Adaptation effect was absent. (5) Secondary behaviors such as closing of the eyes and grimacing were observed. The internal model related to cerebellar functions can be modified using feedback-error information. Results suggest that internal model dysfunction caused this patient's stuttering. EDUCATIONAL OBJECTIVES: After reading this text, the reader will be able to: (1) provide characteristics of neurogenic stuttering after the cerebellum infarction; (2) discuss the relationship between neurogenic stuttering and functions of the cerebellum.