Micrographia secondary to lenticular haematoma.
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of Neurology, Neurosurgery, and Psychiatry 1988;51:1353-1356 Two months later a new examination There was no excessive activation or Letters found no weakness on the right side. Sensacocontraction of antagonist muscles, as seen tion, coordination and speech were normal. in dystonia. A new CT brain scan showed a maiomgrsphia e y to nicular bae Tendonjerks were slightly asymmetrical, but linear (antero-posterior) low density lesion matomna not pathologically hyperactive in the right of the left lenticular nucleus (putamen Sir: A focal lesion ofthe lenticular nucleus is limbs. No abnormal postures were seen in mainly) and mild compensatory dilatation of usually associated with hemidystonia, hemithe limbs. Finger counting and repetitive the left anterior horn. (fig, b and c). chorea and Parkinsonism. We describe the finger movements with the right hand, and This patient showed a typical microcase of a patient with a writing difficulty as simultaneous bilateral hand activation were graphic handwriting, similar in every respect the only clinical manifestation of a lenticular all normal. The patient's only difficulty, as to that observed in Parkinson's disease. haemorraghic lesion. he volunteered, consisted in writing. He held Writing is known to be one single, although A 59 year old man with a previous history the pen correctly and initiated writing with a complex, motor program.1 Recent physof hypertension was admitted after develnormal speed and rhythm. However, his caliological studies suggest that motor plans oping right hemiparesis of acute onset. igraphy became progressively smaller as he and simple motor programs are relatively On examination, blood pressure was continued to write, until it was barely underintact in patients with Parkinson's disease;2 210/120 mmHg; facial asymmetry with standable (fig A). At this moment the patient however, there is an abnormal quantitative deviation of the mouth to the left, severe complained of a feeling of tightness in the specification ofthe components of the motor brachial weakness (0/5) and moderate hand, but no abnormal posture was programs.3 The characteristics of the abnor(2-3/5) crural paresis were present. There observed throughout the examination. mality shown by our patient indicate that he was also a speech disorder characterised by Electromyography of the forearm and was capable of adequately selecting and dysarthria with impaired fluency and hand muscles revealed a normal pattern of starting the muscle activity necessary for anomia. Tendon jerks were sluggish in the fast ballistic movements of the right wrist writing, but failed to run the motor right arm and hyperactive in the right leg. (either flexion or extension); movement time sequences adequately. This observation proPlantar response was extensor on the right and reaction time were also normal when the vides further clinical support for the conand flexor on the left side. The rest of same movements were initiated by an tention that the striopallidal complex is the neurological examination was external somaesthetic or auditory cue. involved in the automatic execution of unremarkable. CT of the brain at that time During writing, EMG bursts in opponens simple and complex motor programs.' showed a large left basal ganglia haematoma pollicis, first interosseous, finger flexor and The underlying reasons for lenticular with moderate oedema. The patient recovfinger extensor muscles of the right limb lesions producing a single motor disturbance ered motor function and speech over the were pathologically fractioned and such as writing, or severe movement disornext 2 weeks and was discharged. decreased in amplitude as writing continued. ders such as hemidystonia and hemichorea, non-motor signs (that is psychic akinesia, (g t o t esczw 0-_ p>,,,_ >fP aphasia) or no clinical manifestation at all, are not known. Understanding such an apparent paradox will probably lead to a ffia--' ,e-H--~' M~ cc4t=-'i ' , ~ better knowledge of the basal ganglia functional organisation. E MARTiNEZ-VILA
[1] J C Rothwell,et al. Scaling of the size of the first agonist EMG burst during rapid wrist movements in patients with Parkinson's disease. , 1986, Journal of neurology, neurosurgery, and psychiatry.
[2] M. Hallett,et al. A physiological mechanism of bradykinesia. , 1980, Brain : a journal of neurology.