RESUMEN
The corticospinal tract is not incriminated in decerebrate rigidity (DR). However, this has not yet been proven in humans. We applied transcranial magnetic stimulation (TMS) in a decerebrate patient to support the hypothesis. A patient suffering from pontine hemorrhage with the fourth ventricular extension was admitted unconscious and in a decerebrate posture. Five days later, she regained consciousness but remained in a decerebrate posture. Motor-evoked potentials (MEPs) to TMS were measured 1 week after she had regained consciousness, and this provoked muscle responses in her hands and feet bilaterally. During the follow-up, the patient's muscle tone became persistently flaccid, although her strength increased to varying degrees in different body and limb muscles. She remained bedridden for 3 years after the stroke and could neither turn on the bed by herself nor perform skilled movements using her hands. The findings of TMS confirmed the animal studies in that the mechanism of decerebrate rigidity did not come through a damage of the corticospinal pathway. This also implies that a preserved corticospinal tract function cannot guarantee a good motor recovery in a stroke patient.
Asunto(s)
Estado de Descerebración/fisiopatología , Potenciales Evocados Motores , Estado de Descerebración/etiología , Femenino , Humanos , Persona de Mediana Edad , Actividad Motora , Tractos Piramidales/fisiopatología , Accidente Cerebrovascular/fisiopatología , Estimulación Magnética TranscranealRESUMEN
A 48-year-old woman suddenly lost consciousness as a result of a right rostral pontine tegmentum haemorrhage. The patient presented with decerebrate rigidity (DR) and regained full consciousness 5 days after the initial onset. The patient was given gabapentin 1200 mg/day nasogastrically and her DR significantly improved, although other antiepileptic drugs such as phenytoin and carbamazepine were given in larger dosages to decrease muscle hypertonicity. The patients' preserved consciousness and motor-evoked potentials to transcranial magnetic stimulation indicated a derangement of the extrapyramidal tracts with preservation of the pyramidal tracts. This case report discusses the possible mechanisms of action of gabapentin in DR.
Asunto(s)
Aminas/uso terapéutico , Ácidos Ciclohexanocarboxílicos/uso terapéutico , Estado de Descerebración/tratamiento farmacológico , Ácido gamma-Aminobutírico/uso terapéutico , Aminas/administración & dosificación , Anticonvulsivantes/administración & dosificación , Anticonvulsivantes/uso terapéutico , Hemorragia Cerebral/complicaciones , Ácidos Ciclohexanocarboxílicos/administración & dosificación , Estado de Descerebración/fisiopatología , Femenino , Gabapentina , Humanos , Intubación Gastrointestinal , Persona de Mediana Edad , Puente/patología , Puente/fisiopatología , Factores de Tiempo , Estimulación Magnética Transcraneal/métodos , Resultado del Tratamiento , Inconsciencia/etiología , Inconsciencia/fisiopatología , Ácido gamma-Aminobutírico/administración & dosificaciónRESUMEN
OBJECTIVE: To report a case in which significant hypotension occurred after initiation of tizanidine in a patient using the antihypertensive agent lisinopril. CASE SUMMARY: A 48-year-old woman was admitted due to cerebral hemorrhage at the midbrain and pons, with extension to the fourth ventricle. Consciousness disturbance (Glasgow coma scale 4) with a decerebrate posture improved 5 days after stroke onset. As the BP was fairly high, antihypertensive agents, including lisinopril, were initiated. Three weeks later, the decerebrate rigidity and high BP remained, and tizanidine was initiated to see whether the decrease in muscle tone could facilitate hypertension control and motor recovery. However, the BP dropped dramatically within 2 hours after the first dose of tizanidine. The tizanidine and all of the antihypertensive medications were withdrawn. Tizanidine was used again after her BP had stabilized, but did not produce similar problems. DISCUSSION: A similar event was reported in 2000. The reaction in our patient appeared after tizanidine initiation and improved after both lisinopril and tizanidine were discontinued. According to the Naranjo probability scale, this was classified as a possible drug interaction. This kind of reaction is seldom mentioned as occurring during co-administration with tizanidine. With its characteristics, tizanidine has the potential to compromise hemodynamic stability during concomitant angiotensin-converting enzyme inhibitor use. CONCLUSIONS: Based upon the literature review, the hypotension in this patient was possibly due to the interaction between tizanidine and lisinopril.