Trigeminal Ganglionopathy on Brain Magnetic Resonance Imaging-A Rare Etiology.

This case report describes a 56-year-old man with periorbital swelling and hyperpigmentation on the right side of the face and a hypopigmented patch on the anterior chest.

Encephaloradiculoneuropathy: A Rare Manifestation of COVID-19 Infection.

Neurological complications are being recognized as important outcomes of the coronavirus disease-2019 (COVID-19) pandemic. We report a rare case of both the central nervous system (CNS) and peripheral nervous system (PNS) involvement, encephalitis with polyradiculoneuropathy in a single patient of COVID infection. How to cite this article: Chakor RT, Barvalia PP, Nadaf S, Manjunath V. Encephaloradiculoneuropathy: A Rare Manifestation of COVID-19 Infection. Indian J Crit Care Med 2022;26(5):646-648.

Delayed Post-hypoxic Leukoencephalopathy with Neuroradiological Recovery.

Manjunath V, Nadaf S, Chakor RT. Delayed Post-hypoxic Leukoencephalopathy with Neuroradiological Recovery. Indian J Crit Care Med 2021;25(11):1326-1328.

Clots in COVID: A Case Series.

As the novel coronavirus-2019 (COVID-19) pandemic spreads across the world, early recognition of the spectrum of symptoms and patterns of clinical presentation is crucial for optimal management. Emerging evidence shows that COVID-19 leads to a prothrombotic state and its association with pulmonary thromboembolism is well established. However, clinicians and the vascular community, in particular, should watch out for the nonpulmonary targets of this lethal virus as the failure to do so could give rise to disastrous consequences. The significance of raised D-dimer levels, whether it translates into thrombotic events for all patients and the need for universal oral anticoagulation postdischarge are issues that need urgent answers. We report a case series of five patients with thrombosis involving nonpulmonary sites. How to cite this article: Kaneria MV, Nadaf S, Desai U. Clots in COVID: A Case Series. Indian J Crit Care Med 2021;25(7):817-821.

Synaptic Nuclear Envelope Protein 1 (SYNE 1) Ataxia with Amyotrophic Lateral Sclerosis-like Presentation: A Novel Synaptic Nuclear Envelope Protein 1 (SYNE 1) Gene Deletion Mutation from India.

A 24-year-old female presented with wasting and weakness of both hands and fasciculations over the chin since 12 years, followed by imbalance while walking and speech changes since 10 years. Her 12-year-old sister also had a similar clinical presentation. There were fasciculations over the chin, tongue, hands, back, thighs with wasting and weakness in tongue, and C7, C8, T1 segments in both upper limbs along with bipyramidal signs. There was limb and gait ataxia. Magnetic resonance imaging brain showed pancerebellar atrophy, and electromyography was suggestive of anterior horn cell involvement in bulbar, cervical, thoracic, and lumbar segments. Next-generation sequencing identified a novel likely pathogenic deletion mutation: chr6:152527389_152527399del, c.22711_22721del, and p.Ala7571ArgfsTer4 in exon 125 of synaptic nuclear envelope protein 1 (SYNE1) gene. This mutation leads to frameshift and premature termination of the protein 'Nesprin 1'. Amyotrophic lateral sclerosis-like presentation followed by cerebellar ataxia have been described with SYNE1 ataxia. This unique phenotype and novel deletion mutation of SYNE1 gene is the first case reported from India.

Progressive delayed hemidystonia following clinically mild traumatic brain injury.

A 16-year-old boy presented with progressive left hemidystonia over 3 years. The possibilities of symptomatic hemidystonia due to focal lesions such as infarct (vasculitis), tumours, tuberculoma, arteriovenous malformations or heredodegenerative disorders such as Wilson disease were considered. Imaging showed a peculiar scar involving right basifrontal region extending upto anterior, centromedian and dorsomedial nuclei of thalamus due to blowout fracture of roof of orbit. This scar was responsible for progressive left hemidystonia. On probing the history, it was revealed that patient had sustained a mild traumatic brain injury (mTBI) 3 years ago. Burke-Fahn-Marsden dystonia severity rating scale showed improvement from 19 to 6 after treatment with tablet trihexyphenidyl 16 mg and clonazepam 1 mg. A linear scar reaching upto thalamus due to blowout fracture of roof of orbit following clinically mTBI is unique. Delayed, progressive hemidystonia has been reported following severe head injury, however is less common following clinically mTBI.

Reversible central neural hyperexcitability: an electroencephalographic clue to hypocalcaemia.

A 23-year-old male patient presented with cognitive decline and seizures. Examination revealed Chvostek's and Trousseau's signs. Investigations revealed hypocalcaemia, hyperphosphatemia and normal intact parathyroid hormone levels. Imaging showed calcifications in bilateral basal ganglia, thalamus and dentate nuclei. Interictal electroencephalogram showed theta range slowing of background activity and bilateral temporo-occipital, irregular, sharp and slow wave discharges, which accentuated during hyperventilation, photic stimulation and eye closure. Appearance of epileptiform discharges after eye closure, hyperventilation and photic stimulation may suggest presence of central neural hyperexcitability due to hypocalcaemia. These features may be an equivalent of peripheral neuromuscular hyperexcitability (Chvostek's and Trousseau's signs) that occurs in hypocalcaemia. The clinical and electroencephalographic features completely reversed with correction of serum calcium without antiepileptic medications. It is important for clinicians to recognise these reversible changes, as it can help to avoid misdiagnosis and long-term administration of antiepileptic becomes unnecessary.