Cardiovascular dysautonomia and cognitive impairment in Parkinson's disease (Review).

Cognitive impairment is a prevalent non-motor symptom of Parkinson's disease (PD), which can result in significant disability and distress for patients and caregivers. There is a marked variation in the timing, characteristics and rate at which cognitive decline occurs in patients with PD. This decline can vary from normal cognition to mild cognitive impairment and dementia. Cognitive impairment is associated with several pathophysiological mechanisms, including the accumulation of ß-amyloid and tau in the brain, oxidative stress and neuroinflammation. Cardiovascular autonomic dysfunctions are commonly observed in patients with PD. These dysfunctions play a role in the progression of cognitive impairment, the incidents of falls and even in mortality. The majority of symptoms of dysautonomia arise from changes in the peripheral autonomic nervous system, including both the sympathetic and parasympathetic nervous systems. Cardiovascular changes, including orthostatic hypotension, supine hypertension and abnormal nocturnal blood pressure (BP), can occur in both the early and advanced stages of PD. These changes tend to increase as the disease advances. The present review aimed to describe the cognitive changes in the setting of cardiovascular dysautonomia and to discuss strategies through which these changes can be modified and managed. It is a multifactorial process usually involving decreased blood flow to the brain, resulting in the development of cerebral ischemic lesions, an increased presence of abnormal white matter signals in the brain, and a potential influence on the process of neurodegeneration in PD. Another possible explanation is this association being independent observations of PD progression. Patients with clinical symptoms of dysautonomia should undergo 24-h ambulatory BP monitoring, as they are frequently subtle and underdiagnosed.

Navigating the Complexity of Alternating Hemiplegia in Childhood: A Comprehensive Review.

Alternating hemiplegia of childhood (AHC) is a complex neurodevelopmental disorder characterized by paroxysmal and transient events of unilateral or bilateral paresis, usually occurring before 18 months of age. Mutations in the ATP1A3 gene, mainly p.Asp801Asn, p.Glu815Lys, and p.Gly947Arg at the protein level, are found in around 80% of the individuals with AHC. Interestingly, these mutations reflect the degree of severity of the neurological symptoms (p.Glu815Lys > p.Asp801Asn > p.Gly947Arg). Some channels involved in this disorder are N-type voltage-gated calcium channels, ATP-sensitive potassium channels, and the sodium/calcium exchanger. In this context, the management of AHC should be divided into the treatment of attacks, prophylactic treatment, and management of comorbidities commonly found in this group of individuals, including epilepsy, attention-deficit/hyperactivity disorder, aggressive behavior, cognitive impairment, movement disorders, and migraine. The importance of an integrated approach with a multidisciplinary team, such as neuropsychologists and dietitians, is worth mentioning, as well as the follow-up with a neurologist. In the present study, we propose new diagnostic criteria for AHC, dividing it into clinical, laboratory, supporting, and atypical features. Also, we review the location of the mutations in the ATP1A3 protein of individuals with AHC, rapid-onset dystonia-parkinsonism (RDP) variants, and early infantile epileptic encephalopathy (variants with hemiplegic attack). We also include a section about the animal models for ATP1A3 disorders.

Cocaine-induced Movement Disorder: A Literature Review.

This study aims to describe movement disorders secondary to cocaine use. To our knowledge, while these presentations have been previously reported in the literature, a comprehensive review has not been published yet. We searched six databases from 1986 to 2022 without language restriction. Case reports, case series, and literature reviews have been analysed to find associations between cocaine use and movement disorders. The present study encompasses epidemiology, clinical manifestations, pathophysiology, and diagnostic challenges of abnormal movements associated with cocaine use. This review highlights the importance of proper initial evaluation and investigation taking into account the broad spectrum of differential diagnoses and exclusion of primary movement disorders. The role of the dopaminergic system in movement disorders is reviewed. Cocaine use is associated with movement disorders such as dystonia, parkinsonism, akathisia, and tics. The complex interaction of multiple factors, including other neurological conditions, such as Tourette syndrome, and additional substances of abuse is discussed. The presentation of these manifestations is often heterogeneous and does not follow a specific pattern. In this way, future research is needed to improve our understanding of the pathophysiological mechanisms and develop novel drug targets for these disorders. Increased awareness among the general public and policymakers could translate into reduced stigma and improved care.

Unraveling belly dancer's dyskinesia and other puzzling diagnostic contortions: A narrative literature review.

Belly dancer's dyskinesia (BDD) is characterized by involuntary abdominal wall movements that are rhythmic, repetitive, and dyskinetic. The present study aims to review BDD's etiology, pathophysiology, and management. We searched six databases to locate existing reports on BDD published from 1990 to October 2023 in electronic form. A total of 47 articles containing 59 cases were found. The majority of the patients affected by BDD were female, accounting for 61.01% (36/59) of the cases. The mean and median ages were 49.8 (standard deviation: 21.85) and 52 years (range: 7-85), respectively. The BDD was unilateral in only 3.38% (2/59). The most commonly reported causes associated with BDD were 17 idiopathic, 11 drug-induced, 11 postsurgical procedures, 5 pregnancies, and 4 Vitamin B12 deficiencies. BDD is a diagnosis of exclusion, and other more common pathologies with similar presentation should be ruled out initially. Differential diagnostic reasoning should include diaphragmatic myoclonus, cardiac conditions, truncal dystonia, abdominal motor seizures, propriospinal myoclonus, and functional or psychiatric disorders.

Trazodone-induced parkinsonism in a middle-aged male: A case report.

Introduction: Trazodone is an antidepressant agent approved for treating major depressive disorders and is also prescribed for insomnia due to its sedative effect. In a few cases, trazodone was associated with parkinsonism. Herein, we describe a case of parkinsonism after a brief exposure to a moderate dose of trazodone. Objective: To describe a case of a patient with trazodone-induced parkinsonism in which the diagnosis was suspected after the exclusion of other common and serious causes. Methods: A case report of trazodone-induced parkinsonism. Clinical Case: A 58-year-old male with sleeping problems was prescribed trazodone 50 mg daily at bedtime. The subject doubled the dosage without medical advice a week later. After 14 days of trazodone treatment, he started to experience difficulty in moving his upper limbs and recurrent falling. Neuroimaging, electrodiagnostic studies, and laboratory exams were unremarkable. Trazodone was discontinued, and the patient fully recovered. Noteworthy, the patient developed a recurrence of the motor symptoms with trazodone-rechallenge. Conclusion: Our case showed reversibly induced parkinsonism after a short intake of a moderate dose of trazodone which was prescribed for insomnia. The patient had a complete recovery after trazodone withdrawal. Noteworthy, the symptoms recurred upon trazodone-rechallenge.

Pregabalin-Induced Parkinsonism: Case Report and Review of the Literature.

Pregabalin is an anti-epileptic drug approved for the treatment of neuropathic pain and focal-onset seizures. In a few cases, pregabalin was associated with parkinsonism. We present a case of a 48-year-old female who had hypertension and was on losartan 50 mg/daily. Her general practitioner prescribed pregabalin 150 mg/daily for fibromyalgia-related pain. The subject doubled the dosage without medical advice. After 5 days of the increased dosage, she started to experience difficulty and slowness in movement associated with resting tremors. Neuroimaging, electrodiagnostic studies, and laboratory exams were unremarkable. Secondary parkinsonism was suspected, so pregabalin was discontinued. The subject fully recovered within 7 days. To the authors' knowledge, only 6 cases of pregabalin-induced parkinsonism were reported in the literature. Pregabalin discontinuation was the most common management. All individuals fully recovered after pregabalin withdrawal. The mechanism of pregabalin-induced parkinsonism is not fully understood.

Flapping Tremor: Unraveling Asterixis-A Narrative Review.

Asterixis is a subtype of negative myoclonus characterized by brief, arrhythmic lapses of sustained posture due to involuntary pauses in muscle contraction. We performed a narrative review to characterize further asterixis regarding nomenclature, historical aspects, etiology, pathophysiology, classification, diagnosis, and treatment. Asterixis has been classically used as a synonym for negative myoclonus across the literature and in previous articles. However, it is important to distinguish asterixis from other subtypes of negative myoclonus, for example, epileptic negative myoclonus, because management could change. Asterixis is not specific to any pathophysiological process, but it is more commonly reported in hepatic encephalopathy, renal and respiratory failure, cerebrovascular diseases, as well as associated with drugs that could potentially lead to hyperammonemia, such as valproic acid, carbamazepine, and phenytoin. Asterixis is usually asymptomatic and not spontaneously reported by patients. This highlights the importance of actively searching for this sign in the physical exam of encephalopathic patients because it could indicate an underlying toxic or metabolic cause. Asterixis is usually reversible upon treatment of the underlying cause.

Isolated pseudo­abducens palsy and contralateral occipital headache with thalamic stroke: A case report and mini­review of the literature.

The abducens nerve (sixth cranial nerve) is essential for lateral eye movement, and its malfunction can cause a variety of issues with vision. Pseudo-abducens palsy is a rare neurological condition that causes a limitation in eye abduction, while the abducens nerve is still functioning. Thalamic pain syndrome, a severe complication of cerebrovascular events, presents as intense neuropathic pain provoked by temperature fluctuations. Although thalamic strokes are infrequently associated with ocular abnormalities, some studies suggest an association between isolated pseudo-abducens palsy and thalamic infarctions. The present study describes the case of a 38-year-old male patient with 1-day progressive diplopia and occipital headache who had abducens palsy on the left side as a result of a right thalamic infarction. The patient had a 10-year history of smoking and a 1-year history of hypertension, which was poorly controlled. The diagnosis was supported by a neurological examination, imaging and stroke etiology investigations. The patient recovered well within 5 days, highlighting the good prognosis of an acute thalamic presentation. In addition, a mini-review of the literature was performed and two similar reports were identified upon searching the literature using the Embase, Google Scholar, Lilacs, Medline, SciELO and ScienceDirect databases. On the whole, the present study demonstrates that understanding the complex neuronal connections inside the thalamus is critical for a proper diagnosis and appropriate intervention strategies in patients with thalamic stroke with oculomotor impairments. Further research is required to elucidate the underlying causes and develop treatment techniques for thalamic infarction consequences.

A Narrative Review of Stroke of Cortical Hand Knob Area.

The cortical hand knob region of the brain is a knob-like segment of the precentral gyrus, projecting into the middle genu of the central sulcus. This anatomic landmark is responsible for intricate control of hand motor movements and has often been implicated in motor weakness following stroke. In some instances, damage to this area has been mistaken for peripheral causes of hand weakness. Our article aims to consolidate clinically relevant information on the cortical hand knob area in a comprehensive review to guide clinicians regarding diagnosis and treatment strategies. We conducted a systematic search within the Medline/PubMed database for reports of strokes in the cortical hand knob region. All studies were published electronically up until December 2023. The search was conducted using the keyword "hand knob". A total of 24 reports containing 150 patients were found. The mean and median ages were 65 and 67 years, respectively. Sixty-two percent of the individuals were male. According to the TOAST criteria for the classification of the stroke, 59 individuals had a stroke due to large-artery atherosclerosis, 8 had small-vessel occlusion, 20 had cardioembolism, 25 were determined, and 38 were undetermined. The most common etiologies for stroke in the hand knob area can be attributed to large vessel occlusions, small vessel occlusions, or cardioembolism. Presentations following damage to this area can mimic ulnar, median, or radial neuropathy as well. Our comprehensive review serves as a resource for recognizing and managing stroke in the cortical hand knob area.

Neuroimaging Techniques in Differentiating Parkinson's Disease from Drug-Induced Parkinsonism: A Comprehensive Review.

Neuroimaging can provide significant benefits in evaluating patients with movement disorders associated with drugs. This literature review describes neuroimaging techniques performed to distinguish Parkinson's disease from drug-induced parkinsonism. The dopaminergic radiotracers already reported to assess patients with drug-induced parkinsonism are [123I]-FP-CIT, [123I]-ß-CIT, [99mTc]-TRODAT-1, [18F]-DOPA, [18F]-AV-133, and [18F]-FP-CIT. The most studied one and the one with the highest number of publications is [123I]-FP-CIT. Fludeoxyglucose (18F) revealed a specific pattern that could predict individuals susceptible to developing drug-induced parkinsonism. Another scintigraphy method is [123I]-MIBG cardiac imaging, in which a relationship between abnormal cardiac imaging and normal dopamine transporter imaging was associated with a progression to degenerative disease in individuals with drug-induced parkinsonism. Structural brain magnetic resonance imaging can be used to assess the striatal region. A transcranial ultrasound is a non-invasive method with significant benefits regarding costs and availability. Optic coherence tomography only showed abnormalities in the late phase of Parkinson's disease, so no benefit in distinguishing early-phase Parkinson's disease and drug-induced parkinsonism was found. Most methods demonstrated a high specificity in differentiating degenerative from non-degenerative conditions, but the sensitivity widely varied in the studies. An algorithm was designed based on clinical manifestations, neuroimaging, and drug dose adjustment to assist in the management of patients with drug-induced parkinsonism.

Catatonia as the Presentation of Encephalopathy Associated With Autoimmune Thyroiditis: A Case Report and Literature Review.

Encephalopathy can be associated with autoimmune disorders such as autoimmune thyroiditis, and it can present with a wide range of neuropsychiatric manifestations. However, it rarely presents with catatonia. We present the case of a middle-aged female with Hashimoto's thyroiditis presenting with catatonia. A literature review of previous similar cases highlighting significant points is also included. A 48-year-old female presented to the emergency department with catatonic symptoms that had worsened over the previous 5 days. A similar condition was reported to have occurred and resolved spontaneously 3 months earlier. On examination, the patient appeared uncooperative and unresponsive. She showed typical symptoms of catatonia, with a score of 21 points on the Bush-Francis Catatonia Rating Scale. Routine tests were within normal ranges except for an elevated level of C-reactive protein and an elevated erythrocyte sedimentation rate. Computed tomography, magnetic resonance imaging, and cerebrospinal fluid analysis were all normal. An electroencephalogram showed diffuse delta-theta range slowing with no epileptiform discharges. Lorazepam was initiated but did not control the catatonic symptoms. Re-evaluation revealed thyroid swelling and elevated levels of thyroperoxidase antibodies. IV methylprednisolone was therefore initiated and produced complete resolution of the catatonic symptoms in 4 hours. The patient was discharged and prescribed prednisone 1 mg/kg daily. At follow-up, the patient continued to show complete resolution of the catatonic symptoms. It is noteworthy that the patient developed hypothyroidism 6 months after this catatonic episode for which levothyroxine 50 mcg/d was prescribed. Encephalopathy associated with autoimmune thyroiditis can initially present with catatonic symptoms in euthyroid cases. The mainstay of treatment is steroids which result in complete resolution of the catatonic symptoms.

Deep Brain Stimulation for the Management of Refractory Neurological Disorders: A Comprehensive Review.

In recent decades, deep brain stimulation (DBS) has been extensively studied due to its reversibility and significantly fewer side effects. DBS is mainly a symptomatic therapy, but the stimulation of subcortical areas by DBS is believed to affect the cytoarchitecture of the brain, leading to adaptability and neurogenesis. The neurological disorders most commonly studied with DBS were Parkinson's disease, essential tremor, obsessive-compulsive disorder, and major depressive disorder. The most precise approach to evaluating the location of the leads still relies on the stimulus-induced side effects reported by the patients. Moreover, the adequate voltage and DBS current field could correlate with the patient's symptoms. Implantable pulse generators are the main parts of the DBS, and their main characteristics, such as rechargeable capability, magnetic resonance imaging (MRI) safety, and device size, should always be discussed with patients. The safety of MRI will depend on several parameters: the part of the body where the device is implanted, the part of the body scanned, and the MRI-tesla magnetic field. It is worth mentioning that drug-resistant individuals may have different pathophysiological explanations for their resistance to medications, which could affect the efficacy of DBS therapy. Therefore, this could explain the significant difference in the outcomes of studies with DBS in individuals with drug-resistant neurological conditions.

Three Cases of Myoclonus Secondary to Ciprofloxacin: "Ciproclonus".

OBJECTIVES: Ciprofloxacin is a fluoroquinolone that is used for bacterial infections involving different systems. In some cases, ciprofloxacin was reported to induce myoclonus. METHODS: We performed a chart review of 3 patients with myoclonus secondary to ciprofloxacin and reviewed the literature for similar cases. Written consent for publication was obtained from each patient, and their identities were concealed for ethical reasons. RESULTS: We describe 3 cases of myoclonus secondary to ciprofloxacin, 2 males and a female aged 61, 26, and 48 years, respectively. The myoclonus appeared within 3 days of ciprofloxacin intake. In all 3 cases, ciprofloxacin was prescribed for urinary tract infection. Electroencephalogram and neuroimaging studies were normal and possible causes were excluded. Thus, ciprofloxacin was believed to be the underlying cause and hence it was withdrawn. The patients had complete recovery on follow-up. CONCLUSIONS: Although ciprofloxacin is widely prescribed for different infections, only 13 cases were reported to develop myoclonus secondary to ciprofloxacin. The mean age of patients was 62 years. Fifty-four percent of cases were males. Cessation of ciprofloxacin was the most common management course. All individuals fully recovered after ciprofloxacin withdrawal. The mechanism of ciprofloxacin-induced myoclonus is probably associated with γ-aminobutyric acid and glutamate pathways.

Somatosensory Auras in Epilepsy: A Narrative Review of the Literature.

An aura is a subjective experience felt in the initial phase of a seizure. Studying auras is relevant as they can be warning signs for people with epilepsy. The incidence of aura tends to be underestimated due to misdiagnosis or underrecognition by patients unless it progresses to motor features. Also, auras are associated with seizure remission after epilepsy surgery and are an important prognostic factor, guiding the resection site and improving surgical outcomes. Somatosensory auras (SSAs) are characterized by abnormal sensations on one or more body parts that may spread to other parts following a somatotopic pattern. The occurrence of SSAs among individuals with epilepsy can range from 1.42% to 80%. The upper extremities are more commonly affected in SSAs, followed by the lower extremities and the face. The most common type of somatosensory aura is paresthetic, followed by painful and thermal auras. In the primary somatosensory auras, sensations occur more commonly contralaterally, while the secondary somatosensory auras can be ipsilateral or bilateral. Despite the high localizing features of somatosensory areas, cortical stimulation studies have shown overlapping sensations originating in the insula and the supplementary sensorimotor area.

Fluoroquinolone-Associated Movement Disorder: A Literature Review.

BACKGROUND: Fluoroquinolones (FQNs) are related to several central nervous system side effects. This review aims to evaluate the clinical-epidemiological profile, pathophysiological mechanisms, and management of FQNs-associated movement disorders (MDs). METHODS: Two reviewers identified and assessed relevant reports in six databases without language restriction between 1988 and 2022. RESULTS: A total of 45 reports containing 51 cases who developed MDs secondary to FQNs were reported. The MDs included 25 myoclonus, 13 dyskinesias, 7 dystonias, 2 cerebellar syndromes, 1 ataxia, 1 tic, and 2 undefined cases. The FQNs reported were ciprofloxacin, ofloxacin, gatifloxacin, moxifloxacin, levofloxacin, gemifloxacin, and pefloxacin. The mean and median age were 64.54 (SD: 15.45) and 67 years (range: 25-87 years). The predominant sex was male (54.16%). The mean and median time of MD onset were 6.02 (SD: 10.87) and 3 days (range: 1-68 days). The mean and median recovery time after MD treatment was 5.71 (SD: 9.01) and 3 days (range: 1-56 days). A complete recovery was achieved within one week of drug withdrawal in 80.95% of the patients. Overall, 95.83% of the individuals fully recovered after management. CONCLUSIONS: Future cases need to describe the long-term follow-up of the individuals. Additionally, FQN-induced myoclonus should include electrodiagnostic studies.

Gepants for Acute and Preventive Migraine Treatment: A Narrative Review.

Calcitonin gene-related peptide (CGRP) antagonists are a class of medications that act as antagonists of the CGRP receptor or ligand. They can be divided into monoclonal antibodies and non-peptide small molecules, also known as gepants. CGRP antagonists were the first oral agents specifically designed to prevent migraines. The second generation of gepants includes rimegepant (BHV-3000, BMS-927711), ubrogepant (MK-1602), and atogepant (AGN-241689, MK-8031). Zavegepant (BHV-3500, BMS-742413) belongs to the third generation of gepants characterized by different administration routes. The chemical and pharmacological properties of this new generation of gepants were calculated. The clinical trials showed that the new generation of CGRP antagonists is effective for the acute and/or preventive treatment of migraines. No increased mortality risks were observed to be associated with the second- and third-generation gepants. Moreover, the majority of the serious adverse events reported probably occurred unrelated to the medications. Interesting facts about gepants were highlighted, such as potency, hepatotoxicity, concomitant use with monoclonal antibodies targeting the CGRP, comparative analysis with triptans, and the "acute and preventive" treatment of migraine. Further studies should include an elderly population and compare the medications inside this class and with triptans. There are still concerns regarding the long-term side effects of these medications, such as chronic vascular hemodynamic impairment. Meanwhile, careful pharmacovigilance and safety monitoring should be performed in the clinical practice use of gepants.

Phenytoin-associated movement disorder: A literature review.

Phenytoin (PHT) was first synthesized as a barbiturate derivative and was approved in 1953 by the Food and Drug Administration. This work aimed to review the pathophysiology, epidemiology, clinical presentation, and treatment of PHT-associated movement disorders (MDs). Studies were searched in relevant databases (ScienceDirect, Google Scholar, Excerpta Medica, Latin American and Caribbean Health Sciences Literature, Medline, and Scientific Electronic Library Online) and were selected by two reviewers irrespective of language between 1963 and 2021. Papers of PHT-induced ataxia alone or tremor were excluded. In total, 127 reports with 219 individuals who developed MDs associated with PHT were encountered. MDs found: 126 dyskinesias, 49 myoclonus, 19 dystonia, 14 parkinsonism, 6 tics, 3 stuttering, and 2 restless legs syndrome. The mean age was 35 years (standard deviation [SD]: 23.5) and the predominant sex was male (53.4%). The mean PHT dose when the MD took place was 370.4 mg (SD: 117.5). A serum PHT concentration was reported in 103 cases, ranging from 4 to 110 µg/mL (median: 27.7 µg/mL). No significant relationship was found between PHT dose and age or PHT level. The mean onset time of PHT-associated MD was 23.4 months (SD: 4.4). The mean recovery time after MD management was 3.7 weeks (SD: 1.1). Regarding management, the most common form was PHT withdrawal in 90.4%. 86.3% of the individuals recovered fully. PHT-induced MD was extensively reported in the literature. Only general terms were used in the majority of the reports. The mechanisms underlying the adverse events caused by PHT probably depend on the presence of predisposing factors.

Lithium-associated movement disorder: A literature review.

In 1949, Cade described "sedative effects" after injecting guinea pigs intraperitoneally with lithium (LTM) carbonate. Based on his experiments, he began treating psychiatric patients with LTM. This literature review aims to evaluate the clinical epidemiological profile, pathological mechanisms, and management of LTM-associated movement disorder (MD). Relevant reports in six databases (Excerpta Medica, Google Scholar, Latin American and Caribbean Health Sciences Literature, Medline, Scientific Electronic Library Online, and ScienceDirect) were identified and assessed by two reviewers without language restriction from 1949 to 2021. A total of 250 reports containing 1100 individuals who developed MD associated with LTM were identified. The MDs encountered 148 parkinsonism (PKN), 114 dyskinesia (DKN), 97 myoclonus, 22 dystonia (DTN), 20 Creutzfeldt-Jakob-like syndrome, 11 akathisia, 10 restless legs syndrome (RLS) symptoms, 6 tics, 5 cerebellar syndromes, and 3 stuttering. In the subgroup of cases not clearly defined, there were 320 individuals with extrapyramidal symptoms, 135 with DTN, 37 with DKN, 24 with PKN, and 7 with RLS. Other 141 individuals were only described as presenting an abnormal involuntary movement without further explanation. The mean age was 53.06 years (standard deviation [SD]: 15.64) and the predominant sex was female, i.e., 56.20% (154/274). The mean LTM dose was 963.03 mg/day (SD: 392.03). The mean serum LTM level was 1.53 mEq/L (SD: 1.08). The median onset time was 3 months (1 day to 40 years). The mean recovery time was 0.94 months (SD: 0.87). 45.94% had a full recovery. LTM-induced MD was extensively reported in the literature. Only general terms were used in the majority of the reports. LTM polytherapy probably affected the identification of the MD cause.

Baclofen and catatonia: a case report.

Baclofen was approved for medical use in the United States in 1977 by Food and Drug Administration. Serious adverse effects associated with this medication are uncommon at usually prescribed doses. Herein, we present a case of baclofen-induced catatonia in a young-adult female with back pain receiving oral baclofen. A 20-year-old female presented to the emergency department with possible seizure-like activity. It was reported that the patient was suffering from acute back pain and was prescribed baclofen three times a day by her general physician one day before her presentation. Upon further discussion, it was known that following an altercation with her family member, she had attempted suicide by consuming 200 mg of baclofen and then developed rapidly progressive symptoms of aphasia, mutism, and decreased oral intake. Laboratory tests, cerebrospinal fluid analysis, and neuroimaging were unremarkable. Electroencephalogram was normal. Bush-Francis Catatonia Rating Scale score was 27. She showed significant improvement following low-dose lorazepam administration. There are four reports in the literature of catatonia secondary to baclofen. The present report is the first to describe the occurrence of catatonia in a previously healthy individual. Analysis of these cases suggests a relationship between a history of psychotic symptoms and catatonia. All the reports were classified as probable by the Naranjo algorithm.