Acute Onset Quadriparesis Research Articles

34-year-old female with acute onset quadriparesis and recurrent carpopedal spasm

Gitelman syndrome is an autosomal recessive condition also characterized by hypokalemic metabolic alkalosis, with hypocalciuria and hypomagnesemia

Clinical and biochemical features of hypokalemic paralysis: a study from rural Eastern India

BackgroundHypokalemic paralysis is characterized by episodic attacks of flaccid muscle weakness of variable duration and severity associated with hypokalemia. Overall, there is a scarcity of data regarding hypokalemic paralysis from Indian subcontinent particularly from rural areas.MethodsA total of 50 consecutive patients of hypokalemic paralysis who were admitted in our hospital were recruited in this study.ResultsFifty patients of hypokalemic paralysis were admitted to our department over a period of 4 years. Forty-two (84%) patients presented with classic acute onset quadriparesis, while eight patients had atypical presentation. Five patients had paraparesis, two had hemiparesis and one patient presented with isolated neck muscle weakness without any limb weakness. Thirty-two patients had primary hypokalemic periodic paralysis (HoPP) and 18 had secondary hypokalemic paralysis. There was no significant difference in severity of weakness (p = 0.53), number of episodes of weakness (p = 0.66) and serum CPK levels (p = 0.36) between primary and secondary hypokalemic paralysis. Secondary cases required significantly prolonged time for recovery as well as higher potassium supplements as compared to the primary HoPP. The severity of weakness of proximal muscles measured in MRC grading showed a significant correlation with serum potassium levels (p = 0.010), but did not show any correlation with CPK Levels (p = 0.86).ConclusionHypokalemic paralysis is an important cause of acute flaccid paralysis in the Emergency Room that often improves dramatically with potassium supplements. While secondary cases often require treatment of underlying etiology, primary hypokalemic paralysis often requires chronic treatment with acetazolamide and/or potassium-sparing diuretics.

A sporadic case of holocord tuberculous transverse myelitis with arachnoiditis

Abstract Background Tubercular infection of the brain and spine is relatively common in endemic regions of the world. Central nervous system tuberculosis can have varied manifestations. The familiar imaging findings are hydrocephalus, ring-enhancing tuberculomas, and meningeal enhancement, having a preference for basal regions. Myelitis is the most common imaging manifestation of spine, with holocord involvement being a rare presentation, as seen in our case. Case presentation We present a case of a pediatric patient undergoing treatment for a tubercular infection of the brain. The patient developed acute onset quadriparesis, manifesting as holocord transverse myelitis on imaging. The imaging findings in the brain manifested as basal meningeal enhancement and non-communicating hydrocephalus, managed by shunt placement. As of the latest, the patient is on follow-up and has a stable disease course. Clinical and laboratory investigations excluded other infectious and non-infectious causes of transverse myelitis, including neuromyelitis optica spectrum disorders. Conclusions Longitudinally extensive transverse myelitis is a rare complication of tubercular myelitis seen as a long-segment signal abnormality with swelling of the cord and corresponding post-contrast enhancement. Involvement of the entire cord is rare, with a handful of cases reported in the literature.

Acute Hypokalemic Paralysis Secondary to Distal Renal Tubular Acidosis Presenting as Guillain Barre Syndrome

A 52 year old female patient presented to emergency casualty with Acute onset quadriparesis with respiratory muscle involvement in. During initial work up Serum electrolytes showed severe hypokalemia. Arterial blood gas showed normal anionic gap metabolic acidosis with positive urine anion gap and urine examination showed alkaline PH in the presence of systemic acidosis. All these findings suggest Distal Tubular Acidosis. Further evaluation revealed strongly positive Anti nuclear antibodies with SS-A also being positive suggesting Sjogren’s Syndrome.

Effectiveness of rehabilitative physiotherapeutic intervention in case of acute onset quadriparesis following transverse myelitis – A case report

Effectiveness of rehabilitative physiotherapeutic intervention in case of acute onset quadriparesis following transverse myelitis – A case report

Pulse corticosteroids for the management of extensive CNS tuberculosis presenting with acute-onset quadriparesis.

Myelopathy in central nervous system tuberculosis is notorious for poor outcomes, determined by the severity of inflammation and cord level involved. Acute-onset quadriplegia or paraplegia in these cases represents a neuro-emergency. We report a young female with disseminated tuberculosis who presented with acute onset flaccid quadriparesis with loss of bladder and bowel function. Imaging helped identify the extensive involvement of the neuraxis. We propose that, in addition to anti-tubercular therapy, high-dose corticosteroids such as pulse methylprednisolone may result in a meaningful improvement and show greater rapidity of response in cases of severe central nervous system inflammation such as arachnoiditis or myelopathy.

The Heart Shape-Sign in the Brainstem

Bilateral medial medullary syndrome is a rare type of stroke, which results due to occlusion of the anterior spinal artery or vertebral artery or its branches. Clinical diagnosis without neuroimaging is very difficult; the characteristic brain MRI finding of “heart appearance” at DWI has been described in bilateral medial medullary infarct. We report the case of 53-year-old man with acute onset quadriparesis. MRI scan of brain, diffusion weighted (DW) imaging revealed heart shaped hyper-intensity areas in the bilateral medial medulla.

The utility of “heart sign” on neuroimaging in acute-onset quadriparesis: A series of three cases

The “heart sign” is a well-described radiological sign in bilateral medial medullary infarction, which is a rare stroke syndrome. It has also been rarely reported in infarction of bilateral paramedian pons and caudal paramedian midbrain. Bilateral brainstem infarcts usually present with varying degree of quadriparesis and in the initial stages, it is difficult to distinguish from other conditions such as Guillain–Barre syndrome and brainstem encephalitis. Recognizing the “heart sign” on magnetic resonance imaging in a stroke-like episode may be helpful in differentiating these conditions from bilateral brainstem infarcts.

Dengue infection and Guillain-barre syndrome

Guillain-barre syndrome (GBS) following dengue infection is quite rare. This case report presents a patient with acute onset quadriparesis, bilateral facial nerve palsy and bulbar involvement associated with the dengue virus infection without any typical symptoms of dengue fever. Clinicians should always keep this association in mind when a patient presents with acute ascending weakness of limbs in the endemic areas even if the patient does not have symptoms suggestive of dengue, because a large number of dengue infections may be asymptomatic.

Fractured cervical facet osteophyte causing acute traumatic myelopathy: Case report

A 52-year-old gentleman presented with acute onset quadriparesis of ten days duration after a trivial fall. Both extremities had grade-2 power. Bilateral hand grip was poor with interossei weakness. The sensation was reduced below C6 with positive Lhermitte’s sign. Deep tendon reflexes were exaggerated except absent bilateral biceps jerk. The bowel and bladder had urgency and frequency. Neck movements were terminally painful. CT and MRI showed a floating bony spicule adjacent to left C5-6 facet joint encroaching the spinal canal causing cord compression. A focal left C5 hemi-laminectomy and foraminotomy were performed. A onecm floating bony spicule adjoining to left C5-6 facet joint was excised. Biopsy ruled out osteochondroma and synovial cyst. The power improved to grade-4 in both extremities with moderate grip and he became dependent ambulatory within three months of surgery. At the end of two years, he recovered almost completely with residual mild left-hand grip weakness.

Guillain–Barré syndrome unmasking asymptomatic peripheral spondyloarthritis

Guillain–Barré syndrome (GBS) is an immune-mediated disease characterized by evolving ascending limb weakness, sensory loss, and areflexia. While moderate and severe back or extremity pain is frequent in patients with GBS due to polyradiculopathy, the literature does not reveal any association of acute demyelinating disorders and asymptomatic sacroiliitis, which becomes symptomatic during the episode of the demyelinating illness. We present the case of a young male patient with acute-onset quadriparesis diagnosed as GBS based on clinical evidence and electrophysiological criteria, who developed acute low backache 7 days after the onset of acute demyelinating illness. Subsequently, a diagnosis of peripheral spondyloarthritis (SpA) was confirmed based on clinical outline (past history of bilateral heel pain and acute low backache), along with magnetic resonance imaging (MRI) and computed tomography findings of focal erosions with surrounding sclerosis on iliac para-articular surface bilaterally. The patient responded well to the therapy (intravenous immunoglobulin, hydroxychloroquine, and symptomatic treatment) thereafter. It is crucial to consider the possibility of SpA when patients with GBS complain of low backache. Timely diagnosis will not only aid in the institution of early therapy but also prevent any long-term sequelae. MRI can visualize active inflammation at sacroiliac joints and spine in recent-onset disease.

General Paresis in a Child with Unusual Presentation

Introduction: Acute onset quadriparesis can be a manifestation of a variety of neurological, metabolic or autoimmune conditions. Rarely, it could be one of many clinical presentations of juvenile dermatomyositis which belongs to the group of idiopathic inflammatory myopathies of childhood. We report the case of a 9-year old girl who presented with global myopathy over a two-month period. Case report: A 9-year-old girl referred with a 2 months history of generalised muscular pain and weakness. There were no significant history of preceded illness, trauma or excessive strenuous exercises. She had no other systemic complaints such as fever or skin rash. Past medical history was unremarkable except for recurrent tonsillitis. Physical examination revealed a child with normal alertness and behaviour. She has notable generalised swelling of all four limbs. Her neurological examination revealed normal tone however her power was definitely reduced in all four limbs (Graded 3/5). She demonstrated signs of proximal myopathy. Subsequent investigations revealed high Creatinine Kinase (CK) levels of 6470U/L, ESR 84mm/hr with deranged transaminases and positive serum mycoplasma and CMV IgM. Her MRI brain and spine along with lumbar puncture results were normal. She was referred to tertiary centre for further evaluation as her weakness progressed. An MRI muscle demonstrated marked inflammation in all four limbs including paravertebral muscles. Her muscle biopsy showed inflammatory myopathy leading to a diagnosis of juvenile dermatomyositis (JDM). She is now showing sustained clinical improvements following a course of immunoglobulin and corticosteroids therapy. Discussion: The diagnosis of JDM is generally considered in patients with rash-associated muscle weakness. Essentially, it involves assessment of muscle, skin, lung and cardiac involvement on top of baseline list of investigations that has been outline by Single Hub and Access point for pediatric Rheumatology in Europe (SHARE). This case reflects that JDM is possible despite non-existent of skin involvement.

Rare Presentations of Spontaneous Spinal Epidural Hematomas in Children.

ABSTRACTSpontaneous spinal epidural hematomas are a rare presentation in children with very few case reports of spontaneous spinal hemorrhage in the pediatric age-group. There has to be a high index of suspicion of spontaneous spinal bleed in patients with acute-onset quadriparesis with no prior history of bleeding or trauma, as early diagnosis and surgical decompression is associated with better neurological outcomes.

Occurrence of Guillain-Barr\xe9 syndrome and Myasthenia Gravis in an elderly male

IntroductionThe occurrence of both Guillain-Barré syndrome(GBS) and myasthenia gravis (MG) in the same individual is rare. The underlying pathophysiology was assumed to be autoimmune humoral mechanisms and molecular mimicry with a cross-reaction between autoantibodies and myelin sheath of peripheral nerves and acetylcholine receptors of the neuromuscular junction (NMJ).Case descriptionA 68-year-old male known diabetic and hypertensive with good drug compliance presented with acute onset quadriparesis with bulbar involvement for 1 day. On examination, he had mild neck flexion weakness and bulbar weakness. He had flaccid quadriparesis with absent deep tendon reflexes and negative Babinski. The rest of the neurological examination was normal.Discussion and evaluationBlood and electrophysiological studies showed evidence of demyelinating polyradiculoneuropathy with temporal dispersion suggestive of Guillain-Barré syndrome. He was treated with intravenous immunoglobin and complete resolution of symptoms. Two months later, he presented with new-onset asymmetrical ptosis and bulbar symptoms for 3 days. On further evaluation, repetitive nerve stimulation showed postsynaptic neuromuscular disorder pattern typical of myasthenia gravis, which was further confirmed by positive acetylcholinesterase receptor antibodies (AChR). Thymoma was ruled out by imaging. He was treated with anticholinesterases, low dose steroids, and immunosuppressants (azathioprine) following which he had improvement of symptoms.ConclusionOur patient, who was initially diagnosed with Guillain-Barré syndrome and recovered, presented 2 months later with a new-onset illness suggestive of myasthenia gravis. This existence of two different neurological entities in the same individual is a rarity, and early recognition is essential for treatment decision and prognostic strategies.

Acute onset quadriparesis following oesophagectomy due to isolated hypophosphataemia.

Acute onset quadriparesis following oesophagectomy due to isolated hypophosphataemia.

A case of acute areflexic, flaccid quadriplegia resulting from acute hypophysitis

Introduction: Acute flaccid paralysis, though relatively common, can pose a diagnostic challenge because of its varied etiology. Case Report: We report a 42-year-old Afro-Caribbean woman whose third and final admission over a 3-week period was because of acute onset quadriparesis. At the final admission, she had flaccid paralysis, no ankle and knee reflexes, and equivocal plantar responses. Investigations revealed severe hypokalemia and hypernatremia, increased creatinine, and low adrenocorticotropic hormone, cortisol, follicle-stimulating hormone, luteinizing hormone, and thyroid-stimulating hormone. She had marked polyuria and increased plasma osmolality. Atrial natriuretic factor was detected and chest computed tomography showed a dilated esophagus and bilateral acute pulmonary emboli. Magnetic resonance imaging revealed an enlarged 1.2x1.4x1.8 cm pituitary gland showing enhancement, indicating hypophysitis. She was diagnosed with quadriparesis secondary to hypokalemia and neurogenic diabetes insipidus secondary to panhypopituitarism involving the stalk, which is postulated to have resulted from acute hypophysitis. She made a complete recovery following treatment with intravenous potassium, fluids and hormone replacement. Conclusion: Hypophysitis-induced panhypo-pituitarism with diabetes insipidus remains a rare cause of quadriparesis.

An Interesting Unusual Case of Hypokalemic Quadriparesis in 48 Years Hypertensive Male Patient: A Liddle's Syndrome

ABSTRACT In 1963, Liddle et al described a disorder that looks like the features of primary aldosteronism, characterized by severe hypertension and hypokalemia but with negligible secretion of aldosterone. They theorized that this was ‘a disorder in which the renal tubles transport ions with such facility that the end result simulates that of a mineralocorticoid excess’. Liddle's syndrome involves abnormal kidney function, with excess reabsorption of sodium and loss of potassium from the renal tubule, and is treated with a combination of low sodium diet and potassiumsparing diuretic drugs (e.g. amiloride). We are reporting a case of 48 years known hypertensive patient admitted with acute onset quadriparesis, ultimately diagnosed as hypokalemia due to Liddle's syndrome, treated with low sodium salt and potassium sparing diuretics-amiloride responds dramatically. How to cite this article Roy MK, Chatterjee A, Sarkar A, Roy K, Lahiri D, Agarwal R, Mukhopadhyay S, Mukhopadhyay J. An Interesting Unusual Case of Hypokalemic Quadriparesis in 48 Years Hypertensive Male Patient: A Liddle's Syndrome. J Postgrad Med Edu Res 2015;49(3):143-145.

A case of type I diabetes mellitus and autoimmune thyroiditis presents with hypokalemic paralysis

Hypokalemic periodic paralysis (HPP) is one form of periodic paralysis, a rare group of disorders that can cause acute onset weakness. Thyrotoxicosis is a well-known cause of periodic paralysis and has to be ruled out when a patient presents with HPP. Here, the authors report a case of recurrent episodes of acute onset quadriparesis attributed to hypokalemia ensuing from autoimmune thyrotoxicosis and he has also been diagnosed with type 1 diabetes mellitus. Although rare, periodic paralysis is to be differentiated from other causes of weakness and paralysis so that the proper treatment can be initiated quickly.

Acute-onset paralysis in a patient of rheumatoid arthritis

Renal tubular acidosis (RTA) is a disorder of renal acidification characterized by inability to acidify urine to pH <5.5 despite the presence of severe systemic metabolic acidosis and hypokalemia. Hypokalemia leads to acute-onset paralysis and may be a presenting manifestation of RTA. Its association with various autoimmune disease has been reported previously in published reports, but has not been much emphasized. We, hereby, report a case of RTA that presented during the flare of rheumatoid arthritis (RA). A 42-year-old female, a known case of RA for 5 years, presented with persistent joint pain for 1 week and acute-onset quadriparesis for 3 days. Primary investigations revealed hypokalemia with metabolic acidosis. She was managed conservatively with potassium supplements and bicarbonate supplements along with steroids and disease-modifying anti-rheumatic drugs. Such a presentation of renal tubular acidosis in a patient during the flare of rheumatoid arthritis is distinctly rare and previously unreported in published studies.

Tenofovir induced Fanconi syndrome: A rare cause of hypokalemic paralysis

We report a 55-year-old female who presented to the emergency department with acute onset quadriparesis. She was diagnosed to have acquired immunodeficiency syndrome 7 years ago and was on tenofovir based anti-retroviral therapy for past 10 months. As the patient also had hypophosphatemia, glucosuria and proteinuria Fanconi syndrome (FS) was suspected. She improved dramatically over next 12 h to regain normal power and also her renal functions improved over next few days. Tenofovir induced FS presenting as hypokalemic paralysis is very rare complication and is the first case reported from India.