Chuen-Der Kao

Hypotension Due to Interaction Between Lisinopril and Tizanidine

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 The tizanidine and all of the antihypertensive medications were withdrawn.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.

Brainstem Excitability is Increased in Subjects with Palmomental Reflex

BACKGROUND/PURPOSE The palmomental reflex (PMR) is a brief contraction of the mentalis muscles caused by a scratch over the thenar eminence, i.e. a brainstem reflex to afferents of upper limb. Using electrophysiologic methods, we studied the characteristics of brainstem excitability in PMR subjects. METHODS Ten healthy PMR subjects were included in the study. Brainstem excitability was assessed with electrical stimulation at the trigeminal nerve, median nerve, ulnar nerve, and sural nerve with recordings at the mentalis muscles. A comparison was made by the probability between the mechanical scratch and the electrical stimulation to evoke the visible muscle contraction of mentalis. RESULTS An electrical stimulus was able to elicit mentalis muscle responses (MMR(electrical)) in all the subjects if the stimulus was of sufficient strength. Using electrical stimulation, the median nerve at the wrist was the best site to evoke MMR(electrical). However, in PMR subjects, the probability of MMR(electrical) to median nerve stimulation was less than that of MMR(scratch), i.e. the clinical findings of PMR. Significantly lower thresholds and higher amplitudes were noted in PMR subjects only when the median nerve was stimulated. The onset latency did not show any difference between the two groups despite the stimulation sites. CONCLUSION The facial motor neurons to median nerve stimulation are more sensitive in PMR subjects. In healthy PMR subjects, this indicates that the excitability increases only in the specific neuronal circuits between the lower cervical spinal cord and the facial motor nucleus in the rostral medulla. MMR(electrical) is a physiologic phenomenon, and PMR is a sign of increased brainstem excitability.

Fatigue as the Only Clinical Manifestation of Colchicine Induced Myopathy

PURPOSE Fatigue may be induced by drug. Here, we reported that patients had fatigue after medication with colchicines. METHOD Eight patients (8 Males, age: 42-72 years old) had fatigue but without weakness as their chief complaints. They all described an inability to maintain a sustained effort, which was ameliorated by rest. RESULTS The course of fatigue was insidious and progressive (mean 3.1 2.3 months, range 1-7 months) along with medication of colchicines (mean 20.3 5.5 months, range 11-28 months). Fatigue severity scale (patient: before drug withdrawal 5.41 0.19; 4 weeks after drug withdrawal 2.46 0.28; control 2.12 0.45) showed fatigue as their most disabling symptom, sometimes preventing them to carry on professional as well as socio-familial activities. The plasma creatine kinase elevated in these 8 patients before withdrawal of colchicines and returned to normal range in each subject 4 weeks after drug withdrawal. A probable diagnosis of drug-induced fatigue was made when symptom subsided after colchicines were discontinued. CONCLUSION It is emphasized that side effect of drug should be considered as a differential diagnosis of fatigue in patients having colchicines. Early recognition and diagnosis will prevent serious muscle damage.

Adult aqueductal stenosis.

Acta Neurologica Taiwanica Vol 16 No 2 June 2007 From the Departments of Neurology, Taichung Hospital, Taichung, Taiwan; Taipei Veterans General Hospital, Taipei, Taiwan; National Yang Ming University School of Medicine, Taipei, Taiwan. Received October 20, 2006. Revised November 20, 2006. Accepted December 18, 2006. Reprint requests and correspondence to: Kwong-Kum Liao, MD. Department of Neurology, Taipei Veterans General Hospital, No. 201, Sec. 2, Shih-Pai Road, Taipei, Taiwan. E-mail: kkliao@vghtpe.gov.tw A 36-year-old woman came to our outpatient department with a chief complaint of two attacks of transient dizziness and soreness pain in nostril followed by right hemiparesis and difficulty in speech, lasting within one hour since one week before. These symptoms got worse when she kept in upright position and were relieved after lying down. She stated that her husband had hit her head many times this year. Neurological examinations revealed no deficit in mentality, attention, cranial nerves, motor and sensory system and also coordination. Initial brain computerized tomography disclosed an obvious supratentorial hydrocephalus with normal size of the fourth ventricle. Lumbar puncture showed an increased opening pressure up to 355 mmH2O. Cerebrospinal fluid (CSF) demonstrated mildly traumatic tapping by 3-tube test. The CSF studies showed values of leukocyte count, cytology, protein and sugar levels all within normal limits. Laboratory tests did not show significant abnormalities in the following data: whole blood cell count, erythrocyte sedimentation rate, serum routine chemistry, titer of antinuclear antibody, rheumatoid factor, and venereal titers. Brain magnetic resonance imaging (MRI) excluded intracranial mass, focal inflammatory or edematous change but enlarged lateral and third ventricles, empty sella and normal fourth ventricular size (Figs. 1-2). Under the impression of aqueductal stenosis (AS), she received ventriculoperitoneal shunting and got sympAdult Aqueductal Stenosis

Subtle brain dysfunction in treated 6-pyruvoyl-tetrahydropterin synthase deficiency: relationship to motor tasks and neurophysiological tests

6-Pyruvoyl-tetrahydropterin synthase (6PTPS) deficiency is a major cause of biopterin deficiency. 6PTPS patients usually have an elevated serum phenylalanine level, a deficiency of neurotransmitters (serotonin and dopamine), and neurological symptoms, if without treatment. We herein investigated the possibility of neurological dysfunction in early-treated patients. In the study, 12 early-treated 6PTPS patients were studied. Their auditory simple reaction time, movement rhythm variation (MRV), somatosensory evoked potentials to median nerve stimulation, and hand muscle responses to transcranial magnetic stimulation, were measured. MRV is a test of repetitive voluntary movements, and was used with and without auditory cues at 0.3 Hz. The 6PTPS patients had an increased motor threshold but normal motor and sensory central conduction times. They performed very well in simple reactions (6PTPS 208.4+/-16.7 ms, control 200.3+/-11.7 ms, p=0.18), but not in continuous tasks. The continuous performance tests showed that MRV had increased in the 6PTPS patients (with cues: 6PTPS 7.35+/-0.94, control 5.47+/-0.80, p<0.0001; without cues: 6PTPS 9.87+/-1.44, control 6.59+/-0.68, p<0.0001). Without cues, MRV had increased in both the 6PTPS and control groups, but more significantly in the 6PTPS patients (6PTPS 2.51+/-0.97, control 1.25+/-0.42; p=0.0001). Our findings indicate that early-treated 6PTPS patients have subtle neurological dysfunctions. They may not maintain movement rhythm as well as normal subjects, even with external cues. Hence, MRV is a good method to assess motor control.

Preserved motor-evoked potentials but without good motor recovery in a patient with decerebrate rigidity

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 patients 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.

Gabapentin for decerebrate rigidity: a case report.

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.