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Recently, there have been some reports regarding hyperkinetic motor behaviours contralateral to hemiplegia in acute stroke.1 2 These behaviours are probably the reflection of early plastic changes of brain maps and circuits after an acute lesion and an active process induced by disinhibition to establish new compensatory pathways.1 I encountered a peculiar case of a patient with right ipsilateral “hypersensation” after a right hemispheric infarction in the acute period who also presented severe left sensorimotor disturbance, hyperkinetic motor behaviours in the right upper limb, anosognosia for hemiplegia, and personal neglect. It was possible to record the patient's subjective experience of the acute phase, which was helpful for understanding the mechanism of anosognosia.
A 76 year old right handed woman was admitted to hospital soon after the onset of left hemiparesis and hemisensory disturbance. She had undergone implantation of a cardiac pacemaker because of sick sinus syndrome. On neurological examination, she was awake and oriented to time and place, but showed inattention and motor impersistence. There was no aphasia or apraxia, but mild left hemispatial neglect was detected. Left hemiparesis was noticed (upper limb 0/5; lower limb 2/5, and face 3/5). Sensory loss was complete in all modalities in the upper limb and severe in the face and lower limb, being slightly preserved for pain and coldness. She denied the existence of left hemiparesis and had completely lost the sensation of ownership of her left hemibody. When I asked her the owner of her left hand and leg while showing them to her, she remarked that these belonged to her grandmother. Brain CT (figure) showed a fresh infarction in the right precentral and postcentral gyrus, extensively extending to the right medial aspect of the frontal lobe (supplementary motor area).
From the second hospital day she complained that she felt very cold in the right half of her body and even sometimes felt pain because the wind from the air conditioner was too strong. I told her that the air conditioning system worked but it was not set at a low temperature because it was winter. She understood my explanation but she continued to complain of spontaneous, abnormal sensation in her right hemibody. The sensation was most severe in the upper limb followed by the face and lower limb, whereas it was not triggered or worsened by any sensory stimulation, and objective sensory deficits were not present in the right hemibody. She usually wrapped herself tightly in a blanket to avoid coldness. She did not complain of any other delusional or illusional feelings. There were also hyperkinetic motor behaviours in the right upper limb such as patting the head with the right arm, manipulations of sheets and blanket, and rhythmic finger movements. The result of a mini mental state examination performed on the fourth hospital day was 25/30.
The abnormal sensation persisted for almost 1 month and gradually subsided, whereas the left hemiparesis and sensory disturbance improved. Touch, pain, and temperature were intact in the face and lower limb, pain and temperature were intact in the upper limb, but there was no improvement in position and vibration in the entire left hemibody. In the meantime, she began to recognise the left hemiparesis and regained the sensation of ownership of her left hemibody. The following are her recollections from the time of onset on the 60th hospital day.
“One morning, I woke up and found that there was a strange hand and foot close to the left side of my body, as though my dead grandmother lay aside me. I tried to throw them off but they were too heavy to move. I glanced at them and felt that they looked flabby and all wrinkled, so I was convinced that they belonged to my grandmother. I had no idea that the left side of my body was disabled or even ill.
After hospitalisation, I felt very cold in the right half of my body and sometimes felt pain because of the powerful wind from the air conditioner. I understood that the hospital did not use cold air conditioning in winter, but that powerful, cold wind could not have come from anything other than an air conditioner. Anyway, this unpleasant feeling gradually subsided, and at the same time, I realised that the disabled left side of my body belonged to me and that I had suffered a brain disorder.”
Ghika et al 1 described 20 patients with hyperkinetic motor behaviours contralateral to hemiplegia in acute stroke who were found only with large infarcts in the territory of the internal carotid artery, middle cerebral artery, or the anterior cerebral artery and which correlated significantly with the severity of motor deficit and the presence of aphasia, neglect, or sensory loss. These characteristics are similar to those in the present patient. However, “hypersensation” as found in this case was not described. Regarding the mechanism of these behaviours, Ghikaet al speculated that they represent the clinical expression of early plastic changes of brain maps and circuits after an acute lesion and probably an active process induced by disinhibition to establish new compensatory pathways.1Such ipsilateral symptoms might occur not only in the motor system, but in the sensory system as well.3 In the present patient, the degree of right hypersensation was parallel with the degree of the disturbance of sensory deficits of the homologous left side, and hypersensation subsided as the sensory disturbance of the left side improved. This suggests that the disinhibition or hyperexcitability to facilitate functional reorganisation may have been the main cause of hypersensation in this case.
Lesional extent must also be considered. Studies in animals and patients with stroke with sensorimotor cortical lesion provided several insights into the basis for recovery. In the cortical region, there are three areas where increased activation has been suggested: the sensorimotor cortex of the unaffected hemisphere, the supplementary motor area (probably bilateral, ipsilateral much greater than contralateral to the lesion), and peri-infarct lesion of affected hemisphere.4-6 In the present case, the right supplementary motor area belonged to the lesion and the right sensorimotor cortex was extensively involved. Acute onset of severe motor and sensory disturbance caused rapid disinhibition and increased activation which had to depend exclusively on the left (unaffected) sensorimotor cortex as the right supplementary motor area and right peri-infarct area could not be involved in the reorganisation process. I speculate that this provoked hyperkinetic motor behaviour as well as hypersensation in the right hemibody.
In the case of patients who recovered, there have been few reports of subjective perceptions in the acute stage of stroke.7 Grotta et al 7 reported the subjective experiences of 24 patients with nonlacunar ischaemic stroke who dramatically recovered. They found that most patients did not recollect the severity of their problem and did not remember important events during the first 24 hours regardless of the side of the lesion. However, as most patients (19 of 24) could clearly recall the exact circumstances involving the onset of their stroke, they speculated that their unawareness of deficit was a form of anosognosia rather than a deficit of memory or global neurological function. The subjective experience of the patient in this study corresponds well with these findings.
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