(g Journal of Neurology, Neurosurgery, and Psychiatry 1988;51:1353-1356 Two months later a new examination There was no excessive activation or found no weakness on the right side. Sensa- cocontraction of antagonist muscles, as seen Letters tion, coordination and speech were normal. in dystonia. A new CT brain scan showed a e lesion y to nicular bae Tendonjerks were slightly asymmetrical, but linear (antero-posterior) low density not pathologically hyperactive in the right of the left lenticular nucleus (putamen matomna Sir: A focal lesion of the lenticular nucleus is limbs. No abnormal postures were seen in mainly) and mild compensatory dilatation of usually associated with hemidystonia, hemi- the 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. he volunteered, consisted in writing. He held Writing is known to be one single, although haemorraghic lesion. 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 devel- normal speed and rhythm. However, his cal- iological 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 under- intact 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 of the components of the motor brachial weakness (0/5) and moderate hand, but no abnormal posture was programs.3 The characteristics of the abnormality shown by our patient indicate that he (2-3/5) crural paresis were present. There observed throughout the examination. was also a speech disorder characterised by Electromyography of the forearm and was capable of adequately selecting and for dysarthria with impaired fluency and hand muscles revealed a normal pattern of starting the muscle activity necessary motor the run to failed but wrist the of writing, right movements ballistic fast the in sluggish anomia. Tendon jerks were proright arm and hyperactive in the right leg. (either flexion or extension); movement time sequences adequately. This observation conPlantar response was extensor on the right and reaction time were also normal when the vides further clinical support for the is and flexor on the left side. The rest of same movements were initiated by an tention that the striopallidal complex of execution automatic the in involved cue. or somaesthetic auditory was external examination the neurological 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 recov- finger 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 disordecreased in amplitude as writing continued. ders such as hemidystonia and hemichorea, next 2 weeks and was discharged. non-motor signs (that is psychic akinesia, aphasia) >f P or no clinical manifestation at all, p >,,,_ t 0-_ o t esczw are not known. Understanding such an apparent paradox will probably lead to a better knowledge of the basal ganglia ' , ~ ffia--' ,e-H--~' M~ cc4t=-'i functional organisation. E MARTiNEZ-VILA J ARTIFDA