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Tizanidine, an α2-adrenergic receptor agonist commonly prescribed as a muscle relaxant, has been associated with limited cases of acute intoxication or withdrawal. Here, we present a case of tizanidine withdrawal in a woman in her 40s who presented with an unusual combination of systemic and neurological symptoms. These included hallucinations, decorticate posture, limb and eyelid tremors, along with hypertension, tachycardia and tachypnoea. The diagnosis of tizanidine withdrawal was established by a comprehensive assessment of the patient’s medical history and the systematic exclusion of other potential diseases. Our approach to managing the withdrawal symptoms was to initiate symptomatic treatment with a combination of a beta-blocker and a calcium channel blocker. Remarkably, this intervention successfully resolved both vital signs and neurological manifestations by the following day. In conclusion, tizanidine withdrawal is associated with a distinct and diagnostically significant neurological syndrome characterised by hallucinations, decorticate posture, tremors and hypersympathetic vital signs. [ABSTRACT FROM AUTHOR]

A primary intraventricular haemorrhage (PIVH) usually presents with non-localised neurological symptoms since the haematoma is limited to the ventricles. However, it is sometimes associated with focal neurological signs, whose pathophysiologies are not confirmed. Here, we report on a case of PIVH who showed rare manifestations in the acute stage: upward gaze palsy and convergence insufficiency. The CT and MRI showed intraventricular haematoma without evidence of parenchymal haemorrhage, local mass effect around midbrain or hydrocephalus. There had been bilateral papilloedema, and it resolved along with improvement of the ophthalmic symptoms, suggesting a possible causal relation to increased intracranial pressure. The ophthalmic abnormalities suggested injury of the rostral part of the midbrain, especially the region around the dorsal midbrain tectum. It should be known that PIVH is one of the causes of acutely developing upward gaze palsy and convergence insufficiency. [ABSTRACT FROM AUTHOR]

We report on a 17-year-old girl with absence status epilepticus who developed recurrent motionless confusional state and continuous generalised 3-4 Hz rhythmic delta waves on electroencephalogram (EEG). The patient had no history of absence, myoclonus or generalised convulsion. Her seizure was resistant to a combination of antiepileptic drugs including carbamazepine. Ictal positron emission tomography using [18F]fluorodeoxyglucose ([18F]FDG-PET) revealed hypermetabolism of the bilateral thalamus and cerebellum and hypometabolism of the frontal, parietal and posterior cingulate cortices. We diagnosed her seizure as absence status and obtained remission by changing medication. The findings of ictal metabolic alteration in previous studies and in our case confirm the pathogenic importance of the thalamus in absence status and that associated cortical deactivation and cerebellar activation may be related to the generation or maintenance of epileptic EEG discharges. [ABSTRACT FROM AUTHOR]