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Najeeb U. Hussain

Najeeb U. Hussain

· Associate Professor

Rutgers University · Psychiatry

Active 2005–2026

h-index3
Citations120
Papers206 last 5y
Funding
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About

Najeeb U. Hussain, MBBS, is an Associate Professor and Vice Chair of Psychiatry at Rutgers New Jersey Medical School, where he also serves as the Director of Clinical Operations in the Department of Psychiatry. He completed his MBBS at Dow Medical College/University of Karachi in 1990 and holds a medical licensure in New Jersey. His areas of interest include Alzheimer's Disease and Schizophrenia. Dr. Hussain's educational background includes a residency in Psychiatry at the University of Missouri Kansas City and a fellowship in Geriatric Psychiatry at UMDNJ/Robert Wood Johnson School of Medicine. He is fluent in Urdu and is affiliated with University Hospital in Newark. His professional focus encompasses clinical practice and research related to psychiatric conditions, with particular attention to geriatric mental health and neurodegenerative disorders.

Research topics

  • Psychiatry
  • Medicine
  • Pediatrics
  • Psychology
  • Internal medicine

Selected publications

  • Functional Neurological Disorder in a Patient With Schizoaffective Disorder

    The Primary Care Companion For CNS Disorders · 2026-04-07

    articleSenior author

    This case of a 54-year-old woman with schizoaffective disorder illustrates how stigma around psychiatric conditions can impact patient disposition, particularly in patient populations with complex neurological disorders.

  • Navigating the intersection of mental health and kidney health: a systematic review of antidepressant safety in renal impairment

    Discover Mental Health · 2025-03-17 · 2 citations

    reviewOpen access

    Depression is a prevalent mental health condition that significantly impacts adults with impaired renal function, yet the safety and efficacy of antidepressants in this population remain inadequately explored. Understanding how renal impairment affects antidepressant pharmacokinetics and clinical outcomes is essential for optimizing treatment strategies. This systematic review adhered to PRISMA 2020 guidelines, conducting a comprehensive literature search across multiple databases, including PubMed, ScienceDirect, ClinicalTrial.gov, and Medline. Studies were included if they evaluated the use of antidepressants in adults with renal impairment, assessing both safety and efficacy outcomes. The review identified 11 studies that met the inclusion criteria, with sample sizes ranging from 30 to 101,409 participants, yielding a total sample size of 192,684. The quality assessment of the included studies was conducted based on the type of study design, focusing on methodological rigor and relevance to the research question. While certain antidepressants demonstrate efficacy, their pharmacokinetic profiles necessitate careful monitoring and dose adjustments in patients with different levels of renal impairment. These insights underscore the need for individualized treatment approaches and highlight areas for future research to enhance care for this vulnerable population.

  • Hyperprolactinemia and Delusion of Pregnancy in Association With Fluphenazine Monotherapy: A Case of a Patient With Schizoaffective Disorder.

    PubMed · 2025-07-31

    articleSenior author
  • Fluoxetine-Induced Extrapyramidal Symptoms

    The Primary Care Companion For CNS Disorders · 2025-10-21 · 1 citations

    articleSenior author
  • Recurrent Catatonia Following Radiation-Induced Hypothyroidism

    The Primary Care Companion For CNS Disorders · 2024

    Senior authorCorresponding
    • Medicine
    • Pediatrics
    • Psychiatry
  • Conceptualizing the relationship between synthetic cannabinoid use and neuroleptic malignant syndrome

    Bipolar Disorders · 2024-09-01

    articleOpen accessSenior author

    Synthetic cannabinoids are an increasingly widespread drug of concern. Given their toxicity and newfound ubiquity, psychiatrists need to be able to manage their adverse effects. They have been linked to exacerbation of certain psychiatric conditions, and we highlight a unique case where neuroleptic malignant syndrome was associated with this. The patient is a 29-year-old female with history of bipolar disorder (multiple past psychiatric admissions) and cannabis/synthetic cannabinoid (SC) use disorder who was recently admitted to an inpatient psychiatric facility for disorganization and agitation. Following this hospitalization, she was discharged on aripiprazole 20 mg daily and lithium 300 mg twice daily. Four days later, she presented to the emergency room following multiple seizure-like episodes and aggressive behavior. Due to ongoing agitation with violence, patient required multiple doses of droperidol, midazolam, hydroxyzine, and was status post administration of soft restraints. The patient's mother described and recorded three episodes of diffuse jerking that lasted 5 min each, with urinary incontinence and oral frothing. Each episode self-resolved, and the patient was conversant throughout episodes with no post-ictal state nor tongue-biting. Neurology was consulted and concluded that her presentation was not consistent with seizures. The patient subsequently was found to have bradykinesia, rigidity, and a rapid increase in creatine kinase from 310 on arrival to a level of 2428 during evaluation- mild neuroleptic malignant syndrome (NMS) was suspected. Her symptoms were thought to be due to use of aripiprazole and droperidol, leading to NMS; however, toxicity from SC's could not be ruled out. Indeed, this was actually suspected, given that the patient had previously been admitted multiple times with similar medication regimens (with higher doses of antipsychotics) without developing NMS. Antipsychotics were discontinued, restraints were avoided as much as possible, and benzodiazepines were instead started for agitation. This resulted in eventual resolution of both her psychiatric and physical symptoms following a short stay in the inpatient unit. Neuroleptic Malignant Syndrome (NMS) is a well-known side effect of potentially all antipsychotics, as antagonism of dopamine receptors lead to drops in neurotransmitter activity within dopaminergic pathways.1 It has a textbook triad of fever, muscle rigidity, and altered mental status (AMS), but in clinical practice, the majority of cases actually present heterogeneously.2 Similarly, synthetic cannabinoids (SC) possess a widely varying drug profile, due to the vast number of derivatives sold. In recent years, SC have become increasingly popular due to their lower cost, easy obtainability and non-detectability on traditional drug screens.3 This is of increasing concern, due to their vastly more unpredictable, severe side-effects compared to cannabis- zero fatalities have been seen with cannabis toxicity, while many have been reported due to SC. Psychiatrically, SC has been show to drastically exacerbate certain conditions including schizophrenia, anxiety, and bipolar disorder. For psychosis in particular, it has been shown that SC use serves as an agonist at cannabinoid type-1 receptors in the brain, leading to acute increases in dopamine.4 NMS and SC use can present very similarly, including increases in CPK, agitation, rigidity, altered mental status, fever etc.1, 4 For our patient, both likely played a role but which contributed more? It is impossible to tell- the former is a clinical diagnosis while SC toxicity cannot be definitively measured.4 Regardless, generalizable takeaways can be made. All patients who require antipsychotics (for bipolar disorder, psychosis etc.) should be screened for concurrent SC use. SC use can precipitate muscle injury, leading to elevations in CPK and consequently rhabdomyolysis. We posit this may lead to lowering the threshold for developing NMS following antipsychotic usage, but even if it does not, combining both will almost certainly lead to worse muscle injury.5 Instead, benzodiazepines and non-dopamine acting drugs should be used unless otherwise necessary. Furthermore, for patients who use synthetic cannabinoids, physical restraints should be minimized, as immobilization drastically increases risk of muscle injury. Both of these points are currently not well-emphasized in the existing literature, but our experience managing patients who present with SC use in an urban, inner-city hospital points towards this being especially important. Many of our patients who present following SC use have acute psychiatric symptoms (aggression, agitation, altered mental status etc.) that require sedation for both their own safety and that of our staff. Choosing the correct form of management is key to reducing their length of stay and morbidity/mortality. We believe that the increasing ubiquity of synthetic cannabinoids, combined with their potential for adverse reactions with existing medications, highlights the need for further molecular research in this area. All authors declare that they have no conflicts of interest. Informed consent was obtained from the patient, and identifiers were anonymized. Ethics approval from our ethics committee was waived due to the manuscript being a case report. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.

  • A clinical complexity of olanzapine use: Peripheral edema

    Bipolar Disorders · 2024 · 1 citations

    Senior authorCorresponding
    • Medicine
    • Psychiatry
    • Psychology

    Olanzapine is a potent atypical antipsychotic, which may lead to peripheral edema. Such edema can affect patients regardless of age, dose, or psychiatric conditions. Due to its rare presentation, this can be difficult to recognize and manage, especially in settings where assessing the patient head-to-toe is less easily done. The patient is a 19-year old boy with a past medical history of bipolar I disorder, benzodiazepine use, and marijuana use disorder who presents after threatening his mother with a knife following an argument with both his parents. At home, he was not taking any prescribed medications. Upon admission to the inpatient psychiatry unit for mood dysregulation, he was started on paliperidone and divalproex sodium and clonazepam daily. Previous trials of risperidone and divalproex sodium were unsuccessful in the past without any side effects. After being admitted, he denied any audiovisual hallucinations/suicidal or homicidal ideation but was superficially cooperative, and his behavior was still erratic, labile, and violent. Indeed, the following day, he punched another patient in the face unprovoked, necessitating the addition of PRN medications (ziprasidone, diphenhydramine, and lorazepam) and being brought to the quiet room. Olanzapine was added and increased due to continued violence (banging his head against a wall and attacking a staff member). In spite of these various medications, the patient expressed poor insight into his condition, in addition to his need for medications and further treatments. Just over a month following the arrival to the unit, the patient developed bilateral upper and lower extremity swelling along with redness. Per the patient, he had noticed such swelling days after he was first given medication in the hospital—however, he did not mention this, nor was it noticed or documented. This swelling manifested as bilateral pitting edema primarily in the lower extremities up to the knee, alongside additional redness of the fingers. The patient denied any associated shortness of breath, rash, pruritus, wheezing, history of allergies/urticaria/asthma and any other medical conditions (cardiac, renal, etc.). Medical workup was initiated, and laboratories were unremarkable besides a mild normocytic anemia. Cardiac and pulmonary physical examinations (and echocardiogram) revealed no pertinent positives, and the patient saturated well on room air throughout. The development of edema can be attributed to the introduction of olanzapine, as seen by its onset a few days after initiation and disappearance following discontinuing the medication. All additional potential causes of the edema including cardiovascular, pulmonary, and allergic were ruled out as shown above. Furthermore, some of the other medications (divalproex sodium, paliperidone) the patient was taking at the time rarely cause edema, and the patient has no past history of such symptoms despite taking them before. Olanzapine was thereafter discontinued and replaced with chlorpromazine, and the patient's legs were elevated, and a trial of compression socks was started. And a week later, the patient's edema had all but subsided and his behavior and mentation were much improved without any aggression or violence. He was thus discharged following a verbal commitment to returning to outpatient treatment, taking his prescribed medications, and controlling his emotions. Olanzapine is a second-generation atypical antipsychotic initially approved for the management of psychotic disorders such as schizophrenia, but later approved for the management of mood disorders such as bipolar disorder and treatment-resistant depression. Pharmacologically, it acts primarily at the serotonin (5H2) and dopamine (D2) receptors in the brain, blocking both.1 Through doing so, in the mesolimbic dopaminergic pathway, olanzapine can help reduce the positive symptoms of psychosis such as hallucinations, delusions, and thought disorganization. However, common side effects of olanzapine include undesired weight gain (and subsequent risk of metabolic effects), sedation (likely secondary to additional antihistamine activity), constipation, and dizziness.2 Premarket trials revealed that peripheral edema, though rare, occurred in approximately 3% of patients taking olanzapine, as opposed to 1% of patients taking a placebo.3 There have been multiple reports delineating such in adults who are receiving olanzapine for the treatment of their psychosis—it has never been described before in an adolescent and only once before in the treatment of bipolar disorder. Prior research has postulated pathways to explain such phenomena, including the vasodilation of blood vessels and subsequent decrease in vascular resistance, due to the additional antagonism of alpha-1 receptors. Regardless of mechanism or specific drug, the development of edema with atypical antipsychotic usage is always managed in a similar manner: discontinuation of the offending agent and switching a well-tolerated, preferably typical antipsychotic (to reduce the likelihood of edema occurring again in the future).3 It has previously been established that edema following olanzapine use can develop within days (as seen with our patient) or even months. Edema can happen at any dose, yet preliminary findings suggest that the risk is higher as the dose increases.4 Although self-limiting and fairly benign, the edema could theoretically have gone on indefinitely if not accidentally noticed. In other words, from a public health perspective, our case illustrated a near miss—it was fortunate that the patient was in the hospital, wearing a short-sleeve gown (which readily exposed the redness and swelling of his hands and forearms). Accordingly, an emphasis on patient education and rapport should be highlighted. The patient should have been made aware of the potential for side effects like this, and if he felt more comfortable with the treatment team, he may have brought up these unwelcome changes on his own. Further complicating matters, it has been well-established previously that adolescent patients tend to be less open to discussing physical changes in their body with healthcare professionals.5 In short, a culture of mutual trust needs to be facilitated so that patients are not only educated about potential complications from the medications they take but also comfortable enough to bring attention to them. If not, this will likely lead to healthcare mistrust and medication noncompliance. Our case also shows the importance of a visual or physical exam, no matter how brief. Patients may be unable to recognize side effects of certain psychiatric medications including edema, weight gain, and rashes. The onus is on the provider to parse them out. Particularly, in an outpatient setting or telepsychiatry though, this can be more difficult due to clothing, less eyes on the patient etc. Here, providers should be aware of these limitations and err toward caution. This presentation is the first to illustrate a rare side effect of olanzapine in an adolescent and the second while treating bipolar disorder. Additional research needs to be done to assess the risk in children and adolescents, given that the possibility in adults is already well-established. Although it is a reversible finding, provider awareness and patient education are key. Patients may not necessarily be able to recognize such symptoms or in certain populations such as adolescents, not as comfortable to discuss them. And in an outpatient or telepsychiatry setting, we believe that doing so as a provider can be even more difficult, necessitating all the more attention. All authors declare that they have no conflicts of interest. Informed consent was obtained from the patient, and identifiers were anonymized. Ethics approval from our ethics committee was waived due to the manuscript being a case report. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.

  • Mania and psychosis associated with right parietal meningioma

    The International Journal of Psychiatry in Medicine · 2019-11-07 · 4 citations

    articleSenior author

    Objective: Meningioma is the most common type of primary central nervous system and intracranial tumor, and psychiatric changes attributed to meningioma include depression, apathy, psychosis, and personality changes. We present a case of a 59-year-old man with right parietal meningioma who developed mania with psychotic features throughout multiple hospitalizations. Method: Single-case report. Results: The patient originally presented with headache and bilateral lower extremity weakness. He was found to have a large medial sphenoidal wing meningioma and a small right parietal meningioma. The sphenoidal wing meningioma was removed via craniotomy, but the right parietal meningioma was not resected. In the following years, the patient developed symptoms of mania and psychosis which coincided with an increase in size of the right parietal meningioma. Conclusions: Previous studies have linked right parietal meningioma to psychosis, but this case is one of the first to suggest that right parietal meningioma may be associated with the development of mania along with psychotic features.

  • Clozapine-Induced Thrombocytopenia in a Patient Non-Naïve to Clozapine

    Psychiatric Annals · 2018-04-01 · 1 citations

    articleSenior author
  • A Forme Fruste Presentation of Neuroleptic Malignant Syndrome Caused by Antipsychotic Medication

    Psychiatric Annals · 2018-05-01 · 2 citations

    articleSenior author

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