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.

Published information about fish botulism is scant. We review here the current literature on fish botulism. Freshwater fish are susceptible to botulism. Only anecdotal evidence exists about possible botulism cases in saltwater fish. With only a few exceptions, the etiology of all cases of fish botulism reported is Clostridium botulinum type E, although fish are sensitive to, and may carry, various C. botulinum types. Clinical signs of botulism in fish include loss of equilibrium and motion, abducted opercula, open mouths, dark pigmentation, and head up/tail down orientation in which attempts to swim result in breaching the surface of the water. Dark pigmentation is thought to be associated with acetylcholine imbalance in botulinum neurotoxin (BoNT)-affected fish. Rarely, but similar to the situation in other animal species, fish can recover from botulism. Fish botulism can cause secondary outbreaks of the disease in birds, as botulism-affected fish stand out from normal fish, and are selectively preyed upon by fish-eating birds, which thus become intoxicated by the BoNT present in sick fish. The source of BoNT in fish has not been definitively confirmed. Fish may ingest C. botulinum spores that then germinate in their digestive tract, but the possibility that fish ingest preformed BoNT from the environment (e.g., dead fish, shellfish, insects) cannot be ruled out. The presumptive diagnosis of botulism in fish is established based on clinical signs, and as in other species, confirmation should be based on detection of BoNT in intestinal content, liver, and/or serum of affected fish.

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.

Guillain-Barré syndrome occurs via molecular mimicry when a trigger sets off an immune response on peripheral nerve epitopes. Patients typically report an antecedent infection, such as an upper respiratory infection or Campylobacter jejuni gastroenteritis. It is typically characterized by progressive, symmetric muscle weakness with absent/decreased deep tendon reflexes. Most cases in the literature report that the paralysis begins in the legs distally and ascends to the extremities. Patients may have sensory symptoms or dysautonomia as well. Notable variant forms include acute motor axonal neuropathy, acute motor/sensory neuropathy, Miller Fisher syndrome, and Bickerstaff brainstem encephalitis. Diagnosis is confirmed if a lumbar puncture shows albuminocytologic dissociation (typically 45 to 200 mg/dL). Nerve conduction studies may also be considered but are not necessary. Management is largely supportive, but intravenous immunoglobulin and/or plasmapheresis for more severe cases may be considered.

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.

Infection with West Nile virus (WNV) is often characterized by a mild febrile illness, but it can progress to meningitis, encephalitis, flaccid paralysis, and respiratory failure. The neuro-ophthalmological manifestations of this disease are uncommonly discussed. This case describes a 49-year-old undomiciled male who developed WNV flaccid paralysis with ophthalmoplegia. His symptoms began with difficulty in walking and progressed over several days to flaccid paralysis and ophthalmoplegia. Cerebrospinal fluid was positive for WNV immunoglobulin M antibodies and electromyography demonstrated acute denervation in several muscle groups. This is an unusual case of neuro-invasive WNV presenting with flaccid paralysis and ophthalmoplegia.

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. .

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.

Apart from the usual differentials of transverse myelitis and cord compression, paraparetic GBS should be considered when sudden, flaccid paralysis of the lower limbs occurs, as prompt diagnosis and management can minimize sequel and unnecessary procedures. We do report a case wherein we managed a similar situation without the use of an immunomodulatory therapy.