Hypermagnesemia is a rare electrolyte abnormality observed in the clinical setting. Patients with this condition can present with a variety of symptoms, depending on the level of serum magnesium. Hypermagnesemia is rarely complicated by weakness of the extremities. We report the case of 32 years old female patient who presented with bilateral upper- and lower-extremity weakness due to hypermagnesemia. Following correction of the serum magnesium level, extremity weakness subsided, and the patient was discharged with improvement. Here, we discuss the delay in the diagnosis and management of this type of clinical presentation.

Hypokalemic periodic paralysis (HPP) is an uncommon condition resulting from channelopathy, impacting skeletal muscles. It is distinguished by episodes of sudden and temporary muscle weakness alongside low potassium levels. The normalization of potassium resolves the associated paralysis. Most of these cases are hereditary. Few cases are acquired and are associated with an etiology related to endocrine disorders (e.g., thyrotoxicosis, hyperaldosteronism, and hypercortisolism). It is characterized by acute flaccid paralysis, usually of the ascending type, affecting the proximal region more than the distal region. Herein, we report the case of a 29-year-old male who instead of the ascending type presented with descending-type acute flaccid paralysis. Potassium level at presentation was 1.7 mEq/L. The patient was managed with parenteral and oral potassium supplementation, after which the weakness was completely resolved.

Hypokalemic periodic paralysis (hypoPP) is a rare channelopathy caused by mutations in skeletal muscle ion channels that usually occurs in young individuals and adolescents. The etiology can be attributed to various factors, such as idiopathic or secondary causes. It is characterized by episodes of sudden flaccid muscle weakness. Timely detection may mitigate the risk of severe complications. Secondary causes of hypoPP, such as hyperthyroidism, should be ruled out, as this could lead to thyrotoxic periodic paralysis. We report the case of a 19-year-old boy who presented to the ED with severe weakness in both the upper and lower extremities. The weakness rapidly progressed to his trunk and was accompanied by acute urinary retention. The physical examination was significant for bilateral upper and lower extremity weakness. Subsequent laboratory investigations revealed markedly low serum potassium levels. The patient\'s symptoms resolved after the replacement of potassium, and he was discharged without neurological deficits. Although rarely accompanied by acute urinary retention, hypoPP must be differentiated from other causes of weakness and paralysis so that the proper treatment can be initiated quickly. The rarity of hypoPP, a condition seldom encountered in clinical practice, and the added rarity of its coexistence with acute urinary retention further underscore the uniqueness of this case report.

Hypokalemic periodic paralysis (HypoPP) is a rare autosomal dominant disease caused by mutations in either calcium or sodium transmembrane voltage-gated ion channels of skeletal muscle or endoplasmic reticulum. Most cases of HypoPP are associated with a mutation in the gene encoding a calcium channel, the CACNA1S gene. Mutations in the channels create leakage currents that disrupt resting potential and depolarize the muscle fiber resulting in transient flaccid paralysis and low extracellular potassium (K+). Patients experience episodes of muscle paralysis typically provoked by exertion and diet. Treatment focuses on the prevention of such episodes with carbonic-anhydrase inhibitors or potassium-sparing diuretics as well as to treatment of acute episodes with oral K+ supplementation. Due to the rarity of the disease, the literature surrounding the disease and pharmacological management is limited. We present a case of two adolescent brothers who present with a confirmed diagnosis of periodic episodes of paralysis and are seeking treatment. Both brothers experience paralytic episodes provoked by acute changes in diet and exercise. However, the lack of literature and treatment guidelines surrounding the disease emphasizes the importance of documenting cases and the effectiveness of treatment outcomes. Additionally, it reminds providers to keep HypoPP on the differential when faced with a young patient experiencing paralytic episodes.

Flaccid paralysis is a neurological syndrome characterized by weakness and paralysis of the limbs, followed by reduced muscle tone. Common causes of flaccid paralysis include blockage of the anterior spinal artery, trauma to the spinal cord, cancer, arterial disease, or thrombosis. A potential differential diagnosis in a 35-year-old male presenting with sudden-onset flaccid paralysis with no history of trauma is hypokalemic periodic paralysis. Treatment with potassium can alleviate symptoms in affected patients. .

BACKGROUND: West Nile Virus is a single-stranded Ribonucleic Acid arbovirus of the Flaviviridae family that is transmitted to humans by Culex species mosquitoes. West Nile Virus infection is asymptomatic in the majority of affected people. Of those who develop symptoms, the usual manifestation is a febrile syndrome, while only 1% develop neurological symptoms due to a neuroinvasive form of infection, including encephalitis, meningitis, asymmetrical flaccid paralysis, or a combination of all these features. Parsonage-Turner syndrome is a rare disorder characterized by sudden painful symptoms and subsequent paralysis, involving a shoulder or one of the upper limbs due to post-infective brachial plexopathy. The etiology is unknown, although it can be considered a multifactorial process: a predisposing factor, such as viral infection or strenuous upper-extremity exercise, can trigger an immune-mediated process localized in the brachial plexus.
METHODS: In late summer, a 79-year-old male Italian patient was admitted to the emergency department for acute right upper limb weakness and high fever, without any mental status impairment, pain, sensory alterations, or signs of meningeal irritation. Laboratory tests confirmed acute West Nile Virus infection, expressed as a unilateral upper limb flaccid paralysis. After a few days, the patient reported an acute pain in the right upper limb scarcely responsive to nonsteroidal anti-inflammatory drug therapy and a subsequent wider distribution of flaccid paralysis. After multiple examinations, Parsonage-Turner syndrome could be suspected. Patient was treated with steroids and reported an improvement of clinical condition after 2 months, with complete pain remission but partial strength recovery in the affected limb.
CONCLUSIONS: West Nile Virus disease has a broad spectrum of neurological manifestations, among which the most common are signs of meningeal irritation or cognitive impairment. We report an unusual presentation of neuroinvasive West Nile Virus infection with arm weakness as expression of unilateral viral neuritis, followed by a post-infective brachial plexopathy consistent with Parsonage-Turner syndrome diagnosis. We diagnosed Parsonage-Turner syndrome after excluding the most common causes of atraumatic acute upper limb pain, through a challenging differential diagnosis in a patient with several comorbidities.

Hypernatremia (serum sodium>160 meq/L) present with diverse neurological manifestations, ranging from flaccid paralysis to impaired cognition, encephalopathy, and even deep coma. Osmotic demyelination refers to changes in brain cells because of an acute change in plasma osmolality. It is further divided into two types, i.e., central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM). Patients with EPM, besides spasticity, may also present with other movement disorders such as catatonia, parkinsonism, and dystonia. We present a case of a postpartum woman bought to the emergency department by her relatives in an unconscious state. In view of poor sensorium (Glasgow coma scale < 7), she was intubated and received mechanical ventilatory support. On admission, computed tomography ofthebrain was normal, and the patient was transferred to the intensive care unit (ICU) for further management. The preliminary work-up in the ICU showed hypernatremia (serum sodium of 182 mEq/L) with hyper-osmolality (359 mOsm/kgH2O). She was managed as per the ICU protocol for hypernatremia. During her ICU stay, her sensorium improved, but she developed flaccid paralysis and was quadriplegic. Thus, a tracheostomy was performed, and she was weaned from the ventilator. After ventilator weaning, she was transferred to the ward for further rehabilitation. During rehabilitation, the patient was able to sit and takefoodorally.To date, only a few cases are reported in postpartum women with acute severe hypernatremia caused by high-grade fever and loss of body fluids leading to extra-pontine demyelination and flaccid paralysis. This case highlightsthat prompt recognition and appropriate intervention can improve the outcomes in these patients.

BACKGROUND: Japanese encephalitis is an arthropod-borne zoonotic flavivirus infection endemic to tropical and subtropical Asia. A minority of infections leads to a symptomatic course, but affected patients often develop life-threatening encephalitis with severe sequelae.
METHODS: Myelitis with flaccid paralysis is a rare complication of Japanese Encephalitis, which-according to our literature search-was reported in 27 cases, some of which were published as case reports and others as case series. Overall, there is a broad clinical spectrum with typically asymmetric manifestation and partly severe motor sequelae and partly mild courses. Lower limb paralysis appears to be more frequent than upper limb paralysis. An encephalitic component is not apparent in all cases CASE PRESENTATION: We herein add the case of a 29 year-old female who developed encephalitis and myelitis with flaccid paralysis during a long-time stay in Indonesia. Diagnostic workup in Indonesia did not clearly reveal an underlying cause. Upon clinical stabilization, the patient was evacuated to her home country Germany, where further diagnostics confirmed Japanese encephalitis virus as the causative agent. The patient has partly recovered, but still suffers from residual paralysis of the upper limb.
CONCLUSIONS: Flaccid paralysis is a rare, and likely underdiagnosed complication of Japanese encephalitis, which, to the best of our knowledge, has never been diagnosed outside endemic areas before.

Guillain-Barré syndrome is the most common cause of flaccid paralysis, with multiple known clinical variants. Autonomic dysfunction, although frequently reported in the clinical course, is often overlooked in the pediatric population and is usually not the initial presenting symptom in this age group CASE PRESENTATION: We present the case of a previously healthy 17-year-old who arrived at the Emergency Department complaining of gastrointestinal symptoms associated with lipothymia. An initial electrocardiogram (ECG) showed sustained sinus bradycardia subsequently associated with arterial hypertension. Structural and inflammatory cardiac pathology were ruled out, as well as auriculoventricular conduction block and posterior reversible encephalopathy syndrome. On the ninth day after initial symptoms, the patient presented sensory and motor nerve disturbances with the cerebrospinal fluid analysis showing a clear albumin-cytologic dissociation, consistent with an atypical presentation of GBS with autonomic dysfunction. Immunoglobulin therapy was administered, developing subsequent aseptic meningitis, that required discontinuation of previous therapy and treatment with plasmapheresis. Clinical improvement was achieved with full motor function recovery.
This case illustrates a Guillain-Barré syndrome variant in which autonomic dysfunction preceded neurologic deficit, a finding uncommon in children, emphasizing this as an important differential diagnosis for severe bradycardia in pediatric patients.

Guillain-Barre syndrome (GBS) is an acute immune-mediated progressive predominantly motor symmetric polyradiculoneuropathy which causes demyelination and leads to weakness, ataxia and areflexia. There are a variety of forms of the syndrome; and despite being the most common cause of acute flaccid paralysis in children, it has a low incidence under 18 years old, and it is even rarer in children less than 2 years of age. Very few cases have been reported under 12 months of age. We describe a case of an 11-month-old male infant presenting with weakness and inability to ambulate who was diagnosed with GBS.