Gabapentin (GBP) is a structural analog of gamma-aminobutyric acid (GABA) that is commonly used in palliative care for symptom management indications including neuropathic pain syndromes, hiccups, cough, and anxiety. An uncommon adverse effect of GBP is urinary incontinence (UI). We report the case of a 61-year-old male with metastatic non-small cell lung cancer who developed probable overflow UI while receiving 1200 mg/day of GBP for chemotherapy-induced peripheral neuropathy. The patient self-tapered GBP to 600 mg/day which resolved the overflow UI, but resulted in poorly controlled bilateral foot pain. The palliative care physician rotated the patient to pregabalin 150 mg/day and his bilateral foot pain improved after his regimen was titrated to 200 mg/day. The patient did not experience overflow UI while taking pregabalin despite the similar pharmacology and comparable doses to GBP. We believe this is the first case report to describe subsequent achievement of pain control by substituting pregabalin without recurrence of UI. Healthcare professionals should consider GBP as a potential cause when evaluating patients presenting with new onset overflow UI.

Gabapentin and pregabalin both exert high affinity to the α2δ subunit of the voltage-gated calcium channels which inhibits excitatory neurotransmitter release. The synergistic mechanism was described in rats given combinations of gabapentin and pregabalin. In this case series, we described 2 cases which may illustrate the synergistic effect of gabapentin and pregabalin in treatment resistant neuropathic pain. Low dose pregabalin was added to therapeutic gabapentin to achieve appreciable pain reduction in one case and improved quality of life in another case. Further research with more enrollment and longer study duration may help elucidate the appropriate dosing and potential associated side effects.

BACKGROUND: Gabapentin is a commonly used medication for neuropathic pain and epilepsy that is prescribed by a wide range of medical specialties. Adverse effects including asterixis and myoclonus have been described in patients with chronic kidney disease, but myokymia has not been previously reported.
METHODS: A 69-year-old man with a history of traumatic brain injury, peripheral neuropathy, amnesia, and posttraumatic stress disorder presented to the hospital after multiple falls attributed to acute onset muscle spasms. He reported taking a total daily dose of 9600 mg of gabapentin, as prescribed. Physical examination demonstrated stimulus-sensitive myoclonus, painful muscle spasms in all extremities, and myokymia in his bilateral calves. Diffuse action tremors, as well as tongue tremors, were also observed.Initial workup, including basic laboratory investigations, brain imaging, and electroencephalogram, was unrevealing. Gabapentin toxicity was suspected, and a gabapentin holiday was initiated with the improvement of myokymia by hospital day 3. The patient was found to have a high gabapentin level (25.8 μg/mL; reference range, 2.0-20.0 μg/mL) measured the morning after hospital presentation. After restarting on a lower dose of gabapentin with multimodal pain control, the patient continued to improve with diminution of his myoclonus, tremor, and gait instability.
CONCLUSIONS: Myokymia is a newly described motor symptom associated with gabapentin toxicity. The mechanism of gabapentin-associated myokymia is currently unknown. A brief medication holiday resulted in the resolution of motor symptoms without significant withdrawal symptoms. Knowledge of this newly reported adverse manifestation can aid physicians in the diagnosis of gabapentin toxicity and prompt treatment, as gabapentin levels are not widely or immediately available.

Gabapentin is an anticonvulsant medication with an indication from the US Food and Drug Administration for use in partial onset seizures and postherpetic neuralgia in the United States. Currently, gabapentin is only classified as a controlled substance subject to stricter prescribing and distributing regulations in certain states, as opposed to pregabalin, an anticonvulsant with a similar mechanism of action which is a considered a Schedule V medication under federal law. Gabapentin shares a structural similarity to pregabalin, and several case reports have suggested that gabapentin has a similar propensity for abuse. The mechanisms of the gabapentin reward pathway, addiction, and withdrawal, however, are not well known. This case report describes a patient with long-term polysubstance abuse and new onset gabapentin dependence and demonstrates the need for increased surveillance of gabapentin prescribing.

BACKGROUND: Antiepileptic drugs (AEDs) are one of the causative drugs of drug-induced hypothyroidism. In most cases, AED-induced hypothyroidism is subclinical and indicated only by abnormalities of free thyroxine (T4) and/or thyroid-stimulating hormone (TSH) levels. Severe symptomatic hypothyroidism following AEDs is rarely reported in the literature.
UNASSIGNED: A 75-year-old man experienced neurologic symptoms including memory impairment, ataxic gait, sensory polyneuropathy and myopathy, lethargy, and edema of the face and lower extremities. He had been administered phenytoin and gabapentin for the treatment of symptomatic traumatic epilepsy 8 years before.
UNASSIGNED: The patient had low free T4 (0.21 ng/dL) and high TSH (113.2 μIU/mL), which indicated hypothyroidism. Negative thyroid-related autoantibody tests and the lack of goiter excluded the possibility of Hashimoto disease. Phenytoin and/or gabapentin were strongly suspected as causing his hypothyroidism.
METHODS: The patient was treated with replacement therapy (levothyroxine 25 μg/day).
RESULTS: His symptoms markedly and promptly improved alongside continued antiepileptic therapy.
CONCLUSIONS: In this case, the patient\'s hypothyroidism was assumed to result from different mechanisms of the 2 AEDs leading to thyroid hormone reduction. AEDs can not only cause asymptomatic thyroid hormone abnormalities but also clinically observable hypothyroidism. Therefore, clinicians should be aware of the association between anticonvulsants and symptomatic hypothyroidism.

Paroxysmal sympathetic hyperactivity is a condition involving a sudden increase in body temperature, heart rate, blood pressure, respiratory rate, sweating, and posturing followed by severe brain injury. Most of the reported preceding disorders involve head trauma, followed by anoxic brain injury, and stroke. Here, we report an extremely rare case of 17-year-old man diagnosed with hemorrhagic arteriovenous malformation, underwent emergent surgery, was on prolonged sedation due to postoperative complications, and subsequently developed paroxysmal sympathetic hyperactivity. We recommend monitoring for paroxysmal sympathetic hyperactivity occurrence with severe brain injury patients, even when sedating.

OBJECTIVE: Hyponatremia induced by antiepileptic drugs is common, but detailed evidence is lacking. This can be problematic for the treating neurologist confronted with a patient with severe hyponatremia in need of an alternative drug. The objective of this study was to examine the association between individual antiepileptic drugs and hospitalization due to hyponatremia.
METHODS: This was a register-based case-control study of patients in the general Swedish population. We included 14,359 individuals with a principal diagnosis of hyponatremia and 57,383 matched controls. The association between newly initiated (≤90 days) and ongoing antiepileptic treatment was investigated using multivariable logistic regression adjusting for concomitant drugs, medical conditions, previous hospitalizations and sociaoeconomic factors.
RESULTS: For newly initiated antiepileptic drugs, adjusted ORs (95% CI) for hospitalization due to hyponatremia, compared to controls, were: carbamazepine 9.63 (6.18-15.33); phenytoin 4.83 (1.14-25.76); valproate 4.96 (2.44-10.66); lamotrigine 1.67 (0.70-4.08); levetiracetam 9.76 (4.02-27.59) and gabapentin 1.61 (1.08-2.38). Newly initiated oxcarbazepine treatment was only found in the hyponatremia group and not in controls. Adjusted ORs (CI) for individuals with ongoing treatment ranged from 7.97 (3.70-18.50) for oxcarbazepine to 0.83 (0.64-1.06) for gabapentin.
CONCLUSIONS: There was a strong association between newly initiated treatment with carbamazepine, oxcarbazepine and levetiracetam, and hospitalization due to hyponatremia. The corresponding association for phenytoin and valproate was moderate. The risk for hyponatremia was lower during ongoing treatment. Lamotrigine and gabapentin had the lowest risk both during initiation and ongoing treatment and may be advantageous in patients at risk of developing hyponatremia.

BACKGROUND Neuromyelitis optica (NMO) is a rare demyelinating disease of the central nervous system; NMO predominantly affects the spinal cord and optic nerves. The diagnosis is based on history, clinical presentation, seropositive NMO-IgG antibody, and notably, exclusion of other diseases. Despite the absence of definitive therapeutic strategies for NMO, methylprednisolone pulse therapy and plasma exchange are used for acute phase treatment, while immunosuppressive agent(s) are recommended to prevent relapses and improve prognosis. Here, we report a repeating relapse NMO case due to lack of regular and maintenance therapy. CASE REPORT A 58-year-old female with chronic NMO presented with a three-day history of new-onset right leg weakness and pain. The patient was diagnosed with NMO three years ago and presented with her fourth attacks. During her initial diagnosis, she was initiated on steroids. One year later, she developed the first relapse and was treated with steroids and rituximab, leading to 1.5-year remission. After the second relapse, steroids and rituximab was still given as maintenance therapy, but was not followed. Thus, the third relapse occurred in five months. During this hospitalization, she received initially high-dose solumedrol (1 g daily for five days) in addition to gabapentin 100 mg (gradually increased to 300 mg) three times a day for muscle spasms. Due to worsening of paresthesia and hemiparesis, it was decided to place her on plasma exchange treatment. After two plasma exchanges, the patient\'s condition was improved and she regained strength in her lower extremity. She completed five more cycles of plasma exchange, and was then discharged on steroid therapy (prednisone 20 mg daily for 10 days then taper) as maintenance therapy and with follow-up in neurology clinic. CONCLUSIONS Over the span of three years, the patient has had three relapses since her NMO diagnosis where her symptoms have worsened. Steroid therapy alone seemed not insufficient in managing her more recent relapses. Nonadherence to NMO treatment likely increased her risk for recurrence, thus regular and long-term maintenance therapy is imperative to delay the progression and prevent relapse in NMO.

The analysis of the case of vulvodynia coexisting with depression. Remission in terms of pain and affective symptoms was achieved simultaneously after including gabapentin in the treatment at a dose of 900 mg/d. Depressive disorders may constitute a risk factor for vulvodynia and occur as a secondary condition to pain. The frequency of other functional pain syndromes such as fibromyalgia and temporomandibular syndrome is much higher in patients with vulvodynia than in the overall female population. The risk of suicide in vulvodynia, similarly to other chronic pain syndromes, is relatively high, especially with coexisting depressive symptoms.

BACKGROUND: Defects in drug metabolic pathways could explain why some patients have a history of multiple adverse drug reactions (ADR); therefore we aimed to analyze genetic polymorphisms in a patient with multiple ADR related to drugs with a common hepatic metabolic pathway through CYP2D6.
UNASSIGNED: We report a patient with psychosis and hypertension related to amitriptyline, tramadol, and duloxetine within a 2-year period.
RESULTS: A pharmacogenetic test was performed to assess the causative role of the CYP2D6 enzyme, but did not demonstrate a metabolic deficiency.
CONCLUSIONS: Although negative results in the reported case; typing for cytochrome P450 isoenzyme polymorphisms could be a useful diagnostic tool in some patients with a history of multiple ADR.