Hyponatremia in the neurocritical care patients is commonly encountered in the setting of either syndrome of inappropriate ADH secretion or cerebral salt wasting. However, differentiation of SIADH and CSW is paramount in view of their divergent treatment strategies. The anaesthetic mandate for a combination of electrocorticography (ECoG) and subcortical motor evoked potential mapping (SCMEPM) substantially differs from that required for each of these monitors in isolation. There is no current consensus defining the anaesthetic management for intraoperative multimodal monitoring combining these two modalities. We report our experience of anaesthetising a drug resistant epileptic patient for craniotomy and resection of his frontal gliotic lesion. We propose a novel anaesthetic technique to cater to the multiple goals of this surgery like optimal neuromonitoring under adequate depth of anaesthesia. We used balanced anaesthesia technique. Continuous intravenous (IV) infusions of Inj. Dexmedetomidine of 1.5 mcg/kg/hour and Inj. Ketamine at 0.5mg/kg/hour were used to supplement inhalational anaesthetic titrated to a MAC up to 0.5. Neuromuscular blockade was avoided after the initial tracheal intubation dose. To the best of our knowledge, this is the first case reporting the safety and efficacy of balanced anaesthetic technique for concurrent ECoG and SCMEPM. Successful intraoperative ECoG and SCMEPM monitoring with absent intraoperative awareness confirmed the safety of our anaesthetic technique. Through this, a composite of patient safety, surgeon satisfaction and adequate intraoperative monitoring could be achieved.To the best of our knowledge, this is the first case reporting the safety and efficacy of balanced anaesthetic technique for concurrent ECoG and SCMEPM. Successful intraoperative ECoG and SCMEPM monitoring with absent intraoperative awareness confirmed the safety of our anaesthetic technique. Through this, a composite of patient safety, surgeon satisfaction and adequate intraoperative monitoring could be achieved. Extracranial vertebral artery aneurysms are a rare cause of embolic stroke; various surgical and endovascular treatment options are available. We report a 44-year-old man with a symptomatic proximal extracranial vertebral artery aneurysm of unclear etiology. The patient presented with brainstem infarction, and the diagnosis of primary extracranial vertebral artery aneurysm was made by computed tomography angiography (CTA). This patient's aneurysm was definitively treated using an endovascular approach with placement of a covered stent in the right proximal vertebral artery. Although aneurysms of this location are traditionally repaired with open aneurysmectomy, we show that endovascular treatment can be a safe and effective alternative approach. In the case reported here, primary extracranial vertebral artery aneurysm presenting with embolic stroke was successfully treated with a covered stent. Complete exclusion of the aneurysm from blood circulation is advisable to achieve full resolution of the embolic source.Although aneurysms of this location are traditionally repaired with open aneurysmectomy, we show that endovascular treatment can be a safe and effective alternative approach. In the case reported here, primary extracranial vertebral artery aneurysm presenting with embolic stroke was successfully treated with a covered stent. Complete exclusion of the aneurysm from blood circulation is advisable to achieve full resolution of the embolic source.The chromosome 22q11.2 region is highly susceptible to both microdeletions and microduplications that have been known to be responsible for multiple congenital anomaly disorders. We describe a patient of 22q11.2 duplication syndrome presenting with bilateral ptosis who has normal psychomotor development. Cranial magnetic resonance imaging and electromyography with repetitive nerve stimulation were normal. Chromosome microarray analysis was performed, and the patient was found to have a de novo 2.8 Mb duplication at 22q11.21. To our knowledge, bilateral ptosis and normal psychomotor development with 22q11.2 duplication syndrome has not been described. The 22q11.2 duplication syndrome should be considered in the differential diagnosis of ptosis. This case report contributes to an expanding clinical spectrum of patients with 22q11.2 duplication syndrome.Blepharoptosis (ptosis) is classified, based on etiology, into mechanical, cerebral, neurogenic, neuromuscular, myogenic, and due to miscellaneous causes. Primary myopathic diseases are rare causes of blepharoptosis and many patients with myogenic ptosis undergo a series of extensive investigations before a myopathy is being considered. In this study, we report four patients with different myopathic disorders who had blepharoptosis as a presenting symptom of their disease. Moreover, we highlight frequent diagnostic errors and difficulties in patients with myopathies who present blepharoptosis. Lack of clear cut aggravation of symptoms by fatigue and response to cholinesterase inhibitors treatment, the association of proximal, distal or extraocular muscle weakness, and positive family history or evidence of a multi systemic disorder should prompt evaluation of an underlying myopathy.A 54-year-old woman presented with a 1-month history of pain and numbness in both feet. She had taken metronidazole for over 4 years previously to treat vaginitis. On nerve conduction studies (NCS), neither the sural nor right superficial peroneal nerve (SPN) was evoked, nor did the left SPN have small amplitude, suggesting axonal peripheral polyneuropathy with sensory fiber involvement. When she restarted metronidazole, she immediately complained of recurrent paresthesia of the feet. We performed three electromyography (EMG) studies and followed the patient for 6 months.We report about two young males who developed significant proximal weakness of all four limbs secondary to intracranial hypertension due to intracranial venous sinus thrombosis. Intracranial venous sinus thrombosis can manifest in a variety of ways which includes isolated intracranial hypertension, focal neurological symptoms or signs and acute or subacute encephalopathy. Various false localising signs have been reported to occur in patients with raised intracranial pressure including cranial nerve palsies and extensive radiculopathy. In a patient presenting with flaccid areflexic quadriparesis and papilledema, the possibility of a potentially reversible dysfunction of the cranial nerves and spinal nerve roots due to a marked rise in intracranial and intraspinal pressure must be recognised. Lumboperitoneal shunt to reduce the intraspinal pressure on the spinal nerve roots has been advocated to reverse the symptoms of extensive radiculopathy in such patients. EHT 1864 clinical trial Both of our patients showed remarkable improvement in symptoms and signs with medical treatment of CVT.