Anti-N-methyl-D-aspartate receptor encephalitis (anti-NMDAR encephalitis) is an autoimmune encephalopathy increasingly recognized in the pediatric population. Although conventional immunotherapy-focused treatments have significantly improved outcomes, a substantial proportion of patients experience enduring neuropsychiatric and cognitive sequelae. Here, we present a three-year longitudinal follow-up report of a female case with confirmed anti-NMDAR encephalitis, focusing on the neuropsychiatric trajectory and cognitive sequelae management with memantine. A previously healthy 10-year-old girl presented with acute-onset psychotic, affective and cataplexy-like features, primarily such as severe irritability and dysphoria, mixed-type mood fluctuation, affective lability, disorganized speaking and thinking, mutism, visual hallucinations, cognitive regression, dysgraphia, and impulsive behavioral dysregulation. The patient received immunotherapy including intravenous methylprednisolone, intravenous immunoglobulin, and rituximab, as well as concurrent psychotropics, including valproate and olanzapine/aripiprazole. Despite psychiatric improvement in 6 months, she showed persistent deficits in memory, executive function, and impulse control, even after 18th month of conventional therapies. Despite appropriate immunotherapy and psychotropic treatments, exhibited persistent deficits in attention, memory, and executive functioning (dysfunction in language and learning), without any severe adverse events. Memantine, a non-competitive NMDAR antagonist with documented neuroprotective properties, was initiated during the chronic phase as complementary to psychotropic medications. While 20 mg/day dose of memantine was administering during 6 months, marked improvement was observed in her verbal fluency, academic functioning, and social engagement, that may be associated with post-acute initiation of memantine alongside conventional treatments. This case highlights the evolving understanding of post-autoimmune cognitive rehabilitation and discusses current evidence and theoretical rationale supporting memantine use in complementary treatment of prolonged cognitive dysfunction in the pediatric anti-NMDAR encephalitis.

Drug-induced acute dystonia is usually associated with combination therapies of neuroleptics, but rarely with the withdrawal or rebound effect of various psychotrops. Very sparse reports have described acute dystonia as a methylphenidate withdrawal (rebound effect), particularly in combination modalities. However, there is no case report or research regarding acute dystonia related to the withdrawal of the short-acting methylphenidate-immediate release form (MPH-IR) in the case of monotherapy of MPH-IR or a combination with guanfacine. Herein, a pediatric case of recurrent acute dystonia with two separate phenomena, locating orolingual and oromandibular/lower extremities, is presented as a withdrawal adverse reaction occurring after abrupt discontinuation of MPH-IR when under a combination therapy with guanfacine. Various options such as anticholinergic agents, re-administrating MPH, or turning to monotherapy from combination modalities, can be suggested in treatment, as well as only hydration may also have the benefit of resolving the symptoms, as in the current case. Practitioners should be aware of all possible adverse effects of MPH, even the rebound effect of short-acting forms.