Bilateral Lower Limb Weakness Research Articles

Navigating the Complexities in Tuberculosis Management: A Case of Transverse Myelitis Masquerade

This case report underscores the intricate nature of diagnosing and treating neurological complications linked with tuberculosis (TB). Initially, a senior male with chronic obstructive pulmonary disease (COPD) was treated for lobar pneumonia, yet failed to show improvement. Further assessment revealed bilateral lower limb weakness and sensory disruptions post Anti Tubercular Therapy (ATT) initiation, suggestive of acute transverse myelitis (ATM). Prompt administration of corticosteroids alongside ATT led to substantial clinical amelioration, despite inconclusive radiological evidence. The case highlights the necessity of considering TB in unconventional neurological presentations, timely initiation of suitable therapy, and the potential benefits of a collaborative approach in enhancing patient outcomes.

A Multidisciplinary Extended Approach to Physiotherapy Rehabilitation in Guillain-Barre Syndrome as Sequelae of COVID-19: A Single Case Study

Introduction: Coronaviruses can cause widespread systemic infections, the most common of which are respiratory complications, which are close to the symptoms of serious acute respiratory syndrome coronavirus (SARS-CoV). Case Description: We report a case of a 16-year-old boy who developed weakness in bilateral lower limbs, difficulty in coughing, and generalized weakness for 2 days. He was diagnosed with post-COVID Guillain-Barre syndrome (GBS). Cerebrospinal fluid (CSF) analysis manifested a CSF protein of 117 mg/dL, a white blood cell count of 6-7/mm3 , and a glucose of too low to comment. Magnetic resonance investigation of the brain revealed mucosal thickening in the bilateral maxillary, ethmoid, and left frontal sinuses. Nerve conduction studies concluded evidence of sensory-motor polyneuropathy. Physiotherapy intervention included patient education, breathing retraining, airway clearance techniques, positioning, a combination of chest proprioceptive neuromuscular facilitation (PNF) techniques, a walking program with supplemented oxygen, and psychological support. Results: Outcome measures have shown enhancement in functional independence and performance of activities of daily living. Conclusion: The evidence from this study suggests that pulmonary rehabilitation plays a pivotal role in managing a patient who is diagnosed with post-COVID GBS, which includes patient education, breathing retraining, airway clearing techniques, a combination of chest PNF techniques, positioning, a walking program with augmented oxygen, and psychological support.

Two homozygous adjacent novel missense mutations in DYSF gene caused dysferlinopathy due to splicing abnormalities.

Background: Dysferlinopathy is an autosomal recessive disorder caused by mutations in the DYSF gene. This study reported two homozygous adjacent missense mutations in the DYSF gene, presenting clinically with bilateral lower limb weakness and calf swelling. Two homozygous adjacent missense mutations in the DYSF gene may be associated with the development of dysferlinopathy, but the exact mechanism needs further investigation. Methods: A retrospective analysis of clinical data from a dysferlinopathy-affected family was conducted. Peripheral blood samples were collected from members of this family for whole-exome sequencing (WES) and copy number variation analysis. Sanger sequencing was employed to confirm potential pathogenic variants. The Human Splicing Finder, SpliceAI, and varSEAK database were used to predict the effect of mutations on splicing function. The pathogenic mechanism of aberrant splicing in dysferlinopathy due to two homozygous adjacent missense mutations in the DYSF gene was determined by an in vivo splicing assay and an in vitro minigene assay. Results: The proband was a 42-year-old woman who presented with weakness of the lower limbs for 2 years and edema of the lower leg. Two homozygous DYSF variants, c.5628C>A p. D1876E and c.5633A>T p. Y1878F, were identified in the proband. Bioinformatics databases suggested that the mutation c.5628C>A of DYSF had no significant impact on splicing signals. Human Splicing Finder Version 2.4.1 suggested that the c.5633A>T of DYSF mutation caused alteration of auxiliary sequences and significant alteration of the ESE/ESS motif ratio. VarSEAK and SpliceAI suggested that the c.5633A>T of DYSF mutation had no splicing effect. Both an in vivo splicing assay and an in vitro minigene assay showed two adjacent mutations: c.5628C>A p. D1876E and c.5633A>T p. Y1878F in the DYSF gene leading to an Exon50 jump that resulted in a 32-aa amino acid deletion within the protein. Point mutation c.5628C>A p. D1876E in the DYSF gene affected splicing in vitro, while point mutation c.5633A>T p. Y1878F in the DYSF gene did not affect splicing function. Conclusion: This study confirmed for the first time that two homozygous mutations of DYSF were associated with the occurrence of dysferlinopathy. The c.5628C>A p. D1876E mutation in DYSF affected the splicing function and may be one of the contributing factors to the pathogenicity.

A rare case of spontaneous spinal epidural hematoma with spontaneous resolution

Spontaneous spinal epidural hematoma (SSEH) is an uncommon cause of acute spinal cord compression. It is a neurological emergency that requires urgent imaging and appropriate treatment to prevent permanent neurological sequelae. Here, we present the case of a 30-year-old male with no known comorbidities who presented to the emergency department with a history of sudden onset of upper backache and chest discomfort followed by bilateral lower limb weakness. On examination, the blood pressure was 220/120 mmHg, and neurological examination showed decreased tone and power of 2/5 in bilateral lower limbs. In view of the initial chest discomfort, a cardiac evaluation was done, which was normal, followed by magnetic resonance imaging of the whole spine, which showed a lesion in the anterior epidural space suggestive of hematoma, causing spinal cord compression. A final diagnosis was C6-T2 dorsal SSEH secondary to a hypertensive emergency.

Unveiling Extramedullary Hematopoiesis: A Case Report Highlighting the Causes, Symptoms, and Management Strategies

Extramedullary hematopoiesis (EMH) serves as a compensatory mechanism in chronic hemolytic anemias, such as thalassemia, and can result in spinal cord compression. This case report highlights a 36-year-old woman with transfusion-dependent β-thalassemia (TDT) who presented with lower extremity motor deficiency, pelvic paresthesia, and bladder dysfunction. The patient had a history of lower back pain, bilateral lower limb weakness, and demonstrated poor compliance with iron chelation therapy. MRI findings indicated spinal cord compression attributable to extramedullary hematopoiesis. Due to the infeasibility of surgical intervention, the patient underwent hypertransfusion and iron chelation therapy. While neurological symptoms improved, urinary retention persisted. The patient continues to receive iron chelation treatment and undergo transfusions. Managing extramedullary hematopoiesis in thalassemia necessitates an individualized treatment approach.

Antidiuretic hormone deficiency secondary to inactive hydrocephalus: a case report

BackgroundDiabetes insipidus is a syndrome characterized by polyuria, which is almost always associated with polydipsia. The most frequent cause is central diabetes insipidus, which is the result of an inadequate secretion of the antidiuretic hormone, and diagnosis involves differentiating it from other causes of polyuria and polydipsia.Case presentationHere, we present a clinical case of a previously healthy 13-year-old Nepali boy, who, in December 2022, was found to have intense polydipsia accompanied by polyuria. He had bilateral lower limb weakness at the time of presentation. Biochemical evaluation demonstrated raised serum sodium (181 mEq/L), serum creatinine (78 μmol/L), and serum uric acid (560 μmol/L) with suppressed serum potassium (2.7 mEq/L), which was the major concern to the clinicians. Further laboratory workup revealed an increased serum osmolarity (393.6 mOsm/kg) with reduced urine osmolarity (222.7 mOsm/kg). On contrast magnetic resonance imaging of the brain, a thick-walled third ventricular cyst with bilateral foramen obstruction, thin membrane-like structure at top of aqueduct of Sylvius with gross obstructive hydrocephalus (inactive), and compressed and thinned pituitary gland with no bright spot was observed. The laboratory findings, radiological findings, and case presentation provided the provisional diagnosis of diabetes insipidus due to hydrocephalus and third ventricular cyst.ConclusionsCentral diabetes insipidus due to hydrocephalus, though rare, can have serious complications including the predilection to develop a deficit of other pituitary hormones. Thus, even if hydrocephalus is dormant with normal intracranial pressure, it must be addressed during investigations of central diabetes insipidus.

A case series of post-infectious chikungunya myeloradiculoneuropathy

Chikungunya fever is an arboviral illness caused by chikungunya virus (CHIKV) and transmitted by the bite of Aedes aegypti and Aedes albopictus. It is an RNA virus belonging to the genus Alphavirus and family Togaviridae. We present a case series of three patients with chikungunya illness developing para/post-infectious myeloradiculoneuropathy.These patients developed neurological symptoms in the form of bilateral lower limb weakness with sensory and bowel involvement after the recovery from the initial acute episode of chikungunya fever. Clinical examination findings suggested myeloradiculoneuropathy with normal Magnetic Resonance Imaging of the Spine, with the nerve conduction study showing sensorimotor axonal polyneuropathy. All the patients were treated with 1 g of methylprednisolone once a day for five days, and case 2 was given intravenous immunoglobulin also. In the follow-up, cases 1 and 2 showed complete recovery without recurrence, and case 3 did not show improvement at one month.

Neuromyelitis Optica Spectrum Disorder (NMOSD) or Chronic-Relapsing Inflammatory Optic Neuropathy (CRION)?: A Challenge in Diagnosis and Treatment

Abstract
 Introduction : Neuromyelitis optica spectrum disorder (NMOSD) is a chronic inflammatory, immune-mediated central nervous system disease targeting the AQP4-water channel membrane protein of the optic nerve and the spinal cord. This case report aims to present a case of seroconverting NMOSD which was initially diagnosed as chronic relapsing inflammatory optic neuropathy (CRION).
 Case Illustration : 15-year-old female with recurrent, steroid-dependent optic neuritis of the LE. During the first attack, brain MRI showed optic nerve inflammation with normal brain findings. Initial test for AQP4-IgG, MOG-Ab and ANA profile were negative. The diagnosis of CRION was made. Treatment with corticosteroid and immunosuppressant agent was maintained for one year. After treatment cessation, however, LE optic neuritis recurred with bilateral lower limb weakness. Spinal MRI showed signs of longitudinal extensive transverse myelitis. Re-testing for AQP4-IgG showed positive result. Diagnosis of NMOSD was made, and the patient was treated with high-dose intravenous corticosteroid followed by oral dose, and immunosuppressant. Final visual acuity of the LE was 1.0, with minimal residual visual field defect and good motor function.
 Discussion : During the initial attack, the patient did not meet the 2015 NMOSD international consensus diagnostic criteria. The AQP4-IgG was negative and no other corresponding signs and symptoms. The criteria was met one year after: optic neuritis, LETM and positive seroconversion of AQP4-IgG.
 Conclusion : Diagnosing NMOSD is at times challenging especially during initial attack. Retesting of the AQP4- IgG is at times necessary in seronegative patients, especially in children showing ADEM-like event with optic neuritis and LETM to achieve diagnosis and proper treatment strategy.

Neuroimaging in uncontrolled hyperglycemia: a case series and literature review

BackgroundThere are wide-ranging differential diagnoses for the myriad of neurological symptoms associated with non-ketotic hyperglycemia. Similarly, various secondary complications of diabetic ketoacidosis present with nonspecific clinical symptoms. These are inadvertently misdiagnosed as epilepsies and strokes with associated hyperglycemia. Direct association between these nonspecific symptoms and hyperglycemia has been proved by demonstrating their resolution with correction of the latter. This case series portrays the spectrum of few rare neuroimaging findings of uncontrolled hyperglycemia, which helps in proper and prompt diagnoses.Case presentationFive diabetic patients with uncontrolled hyperglycemia were observed. Striatal hyperdensity on computed tomography or striatal T1 hyperintensity on magnetic resonance imaging was observed in three patients who presented with movement disorders. The abnormality was bilateral in one case. These observations were consistent with hyperglycemia-induced hemichorea–hemiballismus syndrome. In another patient who had presented with focal seizures, magnetic resonance imaging revealed subcortical T2/FLAIR hypointensity in bilateral occipital regions, which has been described to be characteristic for non-ketotic hyperglycemia-related seizures. Yet another patient who had been treated for diabetic ketoacidosis had developed bilateral lower-limb weakness. In correlation with a background of rapid correction of hyponatremia, magnetic resonance imaging revealed symmetric areas of altered signal intensity in the bilateral perirolandic region showing an open ring pattern of diffusion restriction, suggesting extrapontine myelinolysis.ConclusionsIn all the cases, the clinical differentials were wide. Neuroimaging was mandatory in establishing hyperglycemia as the underlying cause for the movement disorders and seizures. Also, neuroimaging aided in timely identification of extra-pontine myelinolysis, which might have prevented further central pontine involvement in the patient with diabetic ketoacidosis.

Hypokalaemic paralysis due to underlying distal renal tubular acidosis as the first presentation of primary Sjogren’s syndrome: a case report

Sjögren syndrome is a systemic autoimmune disease that primarily affects the exocrine glands. A 36-year-old woman presented with sudden onset of bilateral lower limb weakness. She was noted to have hypokalaemia with a normal anion gap metabolic acidosis. Subsequent investigations revealed high ESR, positive ANA, absent dsDNA, normal C3, C4, positive anti-Ro and negative anti-La. Labial biopsy revealed a lymphocytic infiltrate and renal biopsy revealed tubulointerstitial nephritis. Sjogren’s syndrome rarely (less than 5%) presents for the first time as renal manifestations such as hypokalaemia related paralysis as a result of type I – distal renal tubular acidosis due to the underlying tubulointerstitial nephritis.

A rare case of multiple myeloma of vertebral bodies with cervical canal stenosis

A 70-year-old male patient presented with bilateral lower limb weakness that progressively extended to the upper limbs. This weakness was accompanied by an inability to walk or stand, back pain, followed by paraparesis and paraplegia.

Development of vasogenic cerebral oedema after CT myelogram with nonionic contrast.

Madam, Cerebral edema is fluid accumulation in brain because of a cerebral injury such as trauma, ischemia, hemorrhage, abscess, tumors, and poisoning. Based on the pathophysiology it is divided into three types cytotoxic, interstitial and vasogenic, among which vasogenic edema is the commonest type. [1] Vasogenic edema is a very rare complication of CT myelogram. A 42-year-old female known case of diabetes, hypertension, focal segmental necrotizing glomerulonephritis, and permanent pacemaker in situ for ASD secundum presented in December 2020 to Aga Khan University Hospital with backache and progressive bilateral lower limb weakness. On clinical examination she was conscious, alert, and oriented. She had a power of 4/5 and +2 reflexes in both the right and left upper limb and a power of 0/5 and absent reflexes in both the lower limbs. Patient was advised CSF studies and CT myelogram. CT myelogram was performed after a lumbar puncture at L3-L4 level. Approximately 12 mL of non-ionic water-soluble contrast was administered into the spinal canal. CT myelogram was normal. CSF studies showed raised protein. Within less than twelve hours she developed altered sensorium and decreased consciousness. Contrast-enhanced CT brain was performed which showed diffuse effacement of cortical sulci with poor gray-white matter differentiation as shown in Figure 1. There was crowding at the foramen magnum with evidence of tonsillar herniation as shown in Figure 2 and 3. Diagnosis of CT myelogram-induced cerebral edema was made. The patient received mannitol along with steroid pulse therapy. There was interval resolution of cerebral edema and tonsillar herniation on follow up CT brain (Figure 4 and 5). Endocrinology was taken onboard for the management of her diabetes. Five doses of pulse therapy were given, and after a five-day admission and observation the patient was discharged in stable condition. CT lumbar myelogram is a well-tolerated commonly performed procedure that employs intrathecal contrast to outline the subarachnoid space. The adverse effects of intrathecal contrast injection include nausea, headache, vomiting, and dizziness due to increase pressure in the subarachnoid spaces. Rare contrast-induced neurotoxicity, status epilepticus seizures and aseptic meningoencephalitis has also been reported with intrathecal and intravascular nonionic contrast agents. [3–5] Cerebral edema is also a rare complication of intrathecal contrast injection with few case reports being described in the literature. [2] We are reporting this case so that clinicians are familiar with this uncommon complication of CT myelogram to start early management for better patient outcome.

Application of the International Classification of Functioning, Disability and Health Model in Recurrent Guillain-Barré Syndrome: A Case Report

The present case report utilises the International Classification of Functioning, Disability and Health (ICF) model to assess the health condition and its impact on various health domains of a 46-year-old male who experienced recurrent Guillain-Barré Syndrome (GBS) for the second time within three years. The patient presented with sudden difficulty swallowing solid food and bilateral lower limb weakness, struggling to rise from a sitting position. The report explores the patient’s ICF profile, highlighting the effect of GBS on his daily life and recovery process. The patient’s remarkable recovery can be attributed to several factors, despite the challenges faced. These factors include good socio-economic status, motivation, family support and consistent physiotherapy. Together, these elements played pivotal roles in facilitating the recovery process.

Neuromyelitis optic spectrum disorder following COVID- 19 (ChAdOx1-S) vaccine

Neuromyelitis optic spectrum disorder is an autoimmune demyelinating astro- cytopathy of central nervous system. It has emerged as a distinct clinical entity following the discovery of pathogenic antibody named AQP4-IgG against aquaporin-4 water channels in astrocytes. The clinical spectrum includes optic neuritis, acute myelitis, acute brain stem syndrome, area postrema syndrome, acute diencephalic syndrome and symptomatic cerebral syndrome.This case describes a young male patient who presented with subacute onset painful visual impairment of left eye along with bilateral lower limb weakness and numbness in the background of recent vaccination for covid-19 infection. Examination revealed bilateral papillitis and bilateral flaccid paraparesis with a sensory level at T4 level. Investigations revealed a longitudinally extensive myelitis spanning the entire length of the spinal cord, bilateral optic neuritis, positive serum AQP4-IgG antibodies with negative infective screening and autoimmune profile. Central nervous system demyelination has been observed with all types of covid-19 vaccines.

Ultrasonographic Features of Muscular Weakness and Muscle Wasting in Critically Ill Patients.

Muscle wasting begins as soon as in the first week of one's ICU stay and patients with multi-organ failure lose more muscle mass and suffer worse functional impairment as a consequence. Muscle wasting and weakness are mainly characterized by a generalized, bilateral lower limb weakness. However, the impairment of the respiratory and/or oropharyngeal muscles can also be observed with important consequences for one's ability to swallow and cough. Muscle wasting represents the result of the disequilibrium between breakdown and synthesis, with increased protein degradation relative to protein synthesis. It is worth noting that the resulting functional disability can last up to 5 years after discharge, and it has been estimated that up to 50% of patients are not able to return to work during the first year after ICU discharge. In recent years, ultrasound has played an increasing role in the evaluation of muscle. Indeed, ultrasound allows an objective evaluation of the cross-sectional area, the thickness of the muscle, and the echogenicity of the muscle. Furthermore, ultrasound can also estimate the thickening fraction of muscle. The objective of this review is to analyze the current understanding of the pathophysiology of acute skeletal muscle wasting and to describe the ultrasonographic features of normal muscle and muscle weakness.

Clinical utility of intraoperative direct wave monitoring in patients with pre-operative motor deficits: Case series

Introduction and importanceD-wave (Direct waves) are Motor Evoked Potentials (MEPs) generated by a single transcranial stimulation and captured by attaching an epidural recording electrode caudal to the vulnerable area. Intraoperative neurophysiologic monitoring (IONM) is widely used in neurosurgery to recognize important neurological structures but can be challenging in the pediatric population due to incomplete neural development. Case presentationCase 1: A 48-year-old female presented to the outpatient department with complaints of difficulty walking for the past six months, numbness and weakness in bilateral lower limbs with recurrent falls for the past 1 month. Case 2: A 12-year-old boy presented to the emergency room with a history of inability to use both upper and lower limbs on the right side with tremulousness. Clinical discussionMagnetic resonance imaging (MRI) Spine in the first case revealed a D9-D10 calcified meningioma with significant spinal cord compression. In the second case, MRI Spine showed C1-C2 Intramedullary Space Occupying Lesion (SOL) and was planned for C1-C2 laminectomy with midline myelotomy. The first case was planned for microsurgical excision of the lesion under IONM guidance. The procedure went smoothly. Microsurgical gross total resection (GTR) of the intramedullary SOL under IONM Guidance was done for the second case. Postoperatively, the first patient showed no neurological compromise or complications. In the second case, following surgery, the child recovered gradually from surgery. ConclusionThis case series demonstrates the successful surgical management of two cases of spinal cord tumors through an IONM-guided surgery and the effective use of D waves in such challenging cases.

Abstract 17642: Takotsubo Cardiomyopathy After Guillian Barre Syndrome

Introduction: Guillian Barre Syndrome (GBS) has the potential to cause acute and long-term cardiac effects. Takotsubo Cardiomyopathy(TCM) is a life-threatening manifestation of dysautonomia in patients with GBS, although infrequently reported in the literature. We present a case of TCM in the setting of GBS. Case Presentation: A 54-year-old woman with no past history presented with progressive ascending bilateral lower limb weakness, numbness and paraesthesia following a recent chest infection. On exam, she had reduced motor power and absent deep tendon reflexes. MRI brain was normal. CSF analysis revealed albuminocytologic dissociation(1a). Nerve Conduction Studies(NCS) showed severe sensorimotor polyneuropathy with demyelinating features suggestive of GBS. She was treated with plasmapheresis. The next day, she developed respiratory failure and was hemodynamically unstable with persistent tachycardia and labile blood pressure. ECG showed sinus tachycardia with ST-segment depression(1b). Chest CT was normal. Echocardiogram showed moderate anterolateral hypokinesia with an ejection fraction(EF) of 30%. Coronary angiography showed no significant arterial stenosis, suggesting TCM with a diagnostic TCM score of 59 (1c,1d). She received steroids, furosemide and norepinephrine. Repeat ECG and echocardiogram on day 11 were normal with improved EF (52%).This was followed by a Cardiac MRI which was normal (1e). Discussion: The precise etiology of TCM in GBS is unknown and is believed to be related to a complex interplay of autonomic dysfunction, catecholamine release and inflammation. Although rare, TCM is a fatal complication of GBS, warranting urgent evaluation and management. Sudden onset hemodynamic instability and new onset ECG changes may raise the suspicion of TCM in GBS and must be ruled out. Early diagnosis and treatment can improve the patient’s prognosis.

Abstract 087: Cocaine‐Induced Acute Spinal Cord Ischemia Syndrome

Introduction Acute spinal cord ischemia syndrome (ASCIS) is a rare disease that is thought to comprise roughly only 1.2% of all strokes [1, 2]. These strokes primarily occur in the anterior spinal cord artery (ASA) and/or the posterior spinal cord artery (PCA) territory and can have widely variable clinical presentation. The use of recreational cocaine in young adults is well known to be responsible for acute ischemic and hemorrhagic strokes in individuals who lack other vascular risk factors. What is significantly rarer with few reported cases, however, is cocaine‐related ASCIS as the etiology of non‐traumatic acute spinal cord myelopathy [3‐7]. Methods N/A Results A 40‐year‐old female with a history of type I Diabetes mellitus, bipolar disorder, and polysubstance abuse presented with acute‐onset bilateral lower limb weakness, sensory loss, neck pain, and bladder incontinence. On admission, she reported using intravenous crack cocaine in the evening before admission and experiencing a fall in the bathroom a few hours after. She was unable to move her lower limbs following this fall. On examination, there was flaccid weakness in both lower extremities with decreased pinprick sensation below the T4 level and absent sensation below the thighs on both sides. She had no trauma preceding her symptoms and denied any recent vaccinations or travel history. An urgent CT (computed tomography) scan of the cervical, thoracic, and lumbar spine ruled out any obvious traumatic injury. Her urine drug screen was positive for cocaine, opiate, cannabinoid, and benzodiazepine. MRI (Magnetic Resonance Imaging) of the brain without contrast was unremarkable. MRI of the spine with contrast demonstrated two areas of T2 hyperintensities from C5‐C6 and T4 to the conus with cord expansion. The lesion in the thoracic spinal cord showed contrast enhancement and spared the dorsal column. Lumbar puncture was traumatic and showed elevated protein (>300 mg/dl) as well as elevated glucose (186 mg/dl). CSF studies, including meningitis/encephalitis panel, gram stain and culture, flow cytometry, cytology, and oligoclonal bands were negative. Serum autoimmune myelopathy panel, serum Aquaporin‐4 antibodies and MOG (Myelin Oligodendrocyte Glycoprotein) antibodies were negative. The other etiologies of non‐traumatic myelopathy, including HIV, Treponema pallidum, and HTLV‐I/II antibodies, were negative. A diagnostic spinal angiogram was completed with no evidence of arteriovenous fistula or aortic dissection. She completed five days of plasma exchange without any improvement and was transferred to an acute rehabilitation facility. At four months follow‐up, she continues to be flaccid in her lower limbs and requires a urinary catheter leading to frequent urinary tract infections. Conclusion While cocaine‐related cerebrovascular events are well documented, very few cases of cocaine‐related ASCIS have been described. The mechanism is thought to be multifactorial due vasospasm, cerebral vasculitis, vascular thrombosis, cardioembolism from cocaine‐induced myocardial infarction or cardiomyopathy, and hypertensive surges [9]. Due to the scarcity of these events, the patient outcomes are unclear. Other studies on outcomes of spinal cord ischemia have shown that ASIA Impairment Scale (AIS) score, lesion level, and patient age were the strongest predictors of neurologic and functional outcomes, whereas etiology of the ischemia had no effect on outcomes [10].

Human rabies encephalomyelitis in the background of rabies outbreak in animals in Gelephu, Bhutan, 2023: a case report

BackgroundRabies continues to pose significant public health challenges in many developing countries including Bhutan. A probable case of rabies was admitted to our hospital and its reporting led to the uncovering of an outbreak in domestic and wild animals. We discuss the challenges in the diagnosis and management of rabies in a resource-limited setting.Case presentationA 35-year-old male presented with intermittent fever, bilateral lower limb weakness that was rapidly progressive, urinary incontinence with episodes of palpitations and sweating. He had sustained a Category III bite on the right lower thigh with four bite marks, inflicted by a stray dog. He had received post-exposure prophylaxis with intra-dermal anti-rabies vaccine. On initial examination, the patient was in distress but cooperative for the interview. He had pulse rate ranging from 60 to 100/min with episodes of diaphoresis and palpitations, but with normal capillary blood glucose. In the lower limb, the muscle power was zero with absent tendon reflexes in the lower limb and impaired abdominal reflex below T10 level. He had hyperaesthesia below T8, hydrophobia, aerophobia and photophobia. He had multiple spontaneous fasciculations in both the thighs and right deltoid and these later involved the intercostal muscles, neck and face muscles. He had altered sensorium and desaturation for which he required mechanical ventilation. Polymerase chain reaction for rabies virus was negative in cerebrospinal fluid and saliva. Rabies virus neutralizing antibody was negative in cerebrospinal fluid but had high titres in the serum. He received Human Rabies Immunoglobulin after admission. He was managed in the intensive care unit and died 23 days later. After this case was notified, a rapid response team was deployed in the field, and uncovered rabies outbreak in animals in the locality.ConclusionsThis case called for a serious evaluation of the country’s efforts in achieving zero rabies deaths by 2030. The management of this case identified several critical areas of context-specific interventions in Bhutan. There is also an urgent need to improve diagnostic capabilities at the national reference laboratory and enhance the technical competencies of healthcare workers in the management of dog bite cases.Graphical

Case study of Guillain-Barré syndrome with acute flaccid paralysis

Guillain-Barre syndrome (GBS) is a sudden and a complicated degenerative neurological disorder which can be acute or chronic in nature. Etiology remains unclear, but pathophysiology shows demyelination of spinal nerve roots characterised by symmetrical limb weakness and muscle stiffness. Death is rare. Early diagnosis and prompt treatment should occur in severe cases. Here we discuss a rare case of GBS as paraesthesia and acute flaccid paralysis. This case report focuses on a 9-year-old male patient presenting with c/o progressive muscle weakness and paraesthesia in the lower extremities. The clinical examination revealed bilateral lower limb weakness, absent deep tendon reflexes, and diminished vibration sense, acute flaccid paralysis. Diagnostic evaluations of CT scan of brain and spine and other preliminary tests confirmed the diagnosis of GBS by demonstrating characteristic findings of demyelinating polyneuropathy and elevated protein levels without pleocytosis, respectively. Prompt initiation of intravenous immunoglobulin therapy and supportive measures, such as physical therapy, were implemented. Over a four-week period, the patient showed progressive improvement in muscle strength, starting from the slight movement in fingers and toes. This case report underscores the importance of accurate diagnosis, and timely initiation of appropriate treatment strategies in managing GBS, highlighting the efficacy of intravenous immunoglobulin therapy as a first-line intervention for GBS patients.