scholarly journals On Neuropsychiatric Manifestations of Basal Ganglia Injury: A Report of Three Cases and Literature Review

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Heela Azizi ◽  
Alexander Kilpatrick ◽  
Olaniyi Olayinka ◽  
Olusegun Poopola ◽  
Maleeha Ahmad ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Clinical Evidence ◽  
Psychiatric Symptoms ◽  
Late Onset ◽  
Psychotic Symptoms ◽  
Motor Processing ◽  
Neuropsychiatric Manifestations ◽  
Affective Disturbances ◽  
Visual Disturbances

The basal ganglia have been considered to primarily play a role in motor processing. A growing body of theoretical and clinical evidence shows that in addition to the motor functions the basal ganglia play a key role in perceptual and visual disturbances. This role may be evident in patients with basal ganglia pathology and subsequent manifestation of symptoms that include cognitive, perceptual, and affective disturbances. We present three cases with basal ganglia pathology that demonstrate affective and psychotic symptoms. Two of the cases presented with late onset psychotic disturbances suggesting likely neurological etiologies. The third case presented with treatment refractory psychosis and symptoms that are rare for a diagnosis of schizophrenia. The role of incidental bilateral basal ganglia calcifications in all the cases is discussed. A review of current literature highlighting various neuropsychiatric manifestations of basal ganglia pathologies in various patients with psychiatric symptoms is presented.

scholarly journals Late Onset Bipolar Disorder due to a Lacunar State

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Elena Antelmi ◽  
Margherita Fabbri ◽  
Lucia Cretella ◽  
Maria Guarino ◽  
Andrea Stracciari
Keyword(s):  
Bipolar Disorder ◽  
Basal Ganglia ◽  
Psychiatric Symptoms ◽  
Late Onset ◽  
Type Ii ◽  
Psychiatric Consultation ◽  
Limb Weakness ◽  
Recent Onset ◽  
New Onset

Objective.To describe a patient with a new onset bipolar disorder (BD) type II, secondary to a lacunar state.Background.Poststroke BD is rare and mainly associated with lesion in the prefrontal-striatal-thalamic circuit.Materials and Methods.A 51-year-old woman came to our attention for a mood disorder of recent onset. At 49, she had suffered acute left-sided limb weakness that improved spontaneously four days later. Arterial hypertension was subsequently diagnosed. After 6 months, she began to suffer from alternating brief periods of expansive and elevated mood with longer periods of depressed mood, with a suicide attempt. We performed extensive laboratory and instrumental investigations, as well as, psychiatric consultation, and a cognitive assessment, which was repeated 9 months later.Results.Brain magnetic resonance disclosed leukoaraiosis and a lacunar state of the basal ganglia. Transcranial Doppler showed a patent foramen ovale. A psychiatric consultation led to the diagnosis of BP type II. Neuropsychological evaluation detected deficits in attention/executive functions, verbal fluency, and memory. Nine months later, after specific psychiatric therapy, the psychiatric symptoms were remarkably improved.Conclusion.Our case sheds light on the role of the basal ganglia in mood disorders and the importance of ruling out brain injury in late onset BP.

“organic Personality Disorder” as Part of Early Neuropsychiatric Manifestations in Huntington’s Disease - a Case Report

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
J. Maia
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Psychiatric Symptoms ◽  
Age Of Onset ◽  
Neuropsychiatric Symptoms ◽  
Personality Change ◽  
Psychotic Symptoms ◽  
Autosomal Dominant Disorder ◽  
Neuropsychiatric Manifestations ◽  
Psychiatric Manifestations

Huntington's Disease (HD) is an inherited autosomal dominant disorder characterized by motor, cognitive and psychiatric symptomatology, being considered a paradigmatic neuropsychiatric disorder that includes all three components of the "Triadic Syndromes": dyskinesia, dementia and depression.Firstly described in 1872 as an "Hereditary Chorea" by George Huntington only in 1993 was its responsible gene identified. A person who inherits the HD gene will sooner or later develop the disease. the age of onset, early signs and rate of disease progression vary greatly from person to person.Neuropsychiatric symptoms are an integral part of HD and have been considered the earliest markers of the disease, presenting sometimes more than 10 years before a formal diagnosis is done. Patients may experience dysphoria, mood swings, agitation, irritability, hostile outbursts, psychotic symptoms and deep bouts of depression with suicidal ideation. Personality change is reported in 48% of the cases, with the paranoid subtype being described as the most prevalent. the clinical case presented illustrates a case of HD which started with insidious psychiatric symptoms and an important personality change.Despite a wide number of medications being prescribed to help control emotional, movement and behaviour problems, there is still no treatment to stop or reverse the course of the disease. Furthermore, psychiatric manifestations are often amenable to treatment, and relief of these symptoms may provide significant improvement in patient's and caregivers quality of life.A greater awarness of psychiatric manifestations of HD is essential to an earlier diagnosis and an optimized therapeutic approach.

Late-onset schizophrenia

2020 ◽  
pp. 671-694
Author(s):  
Ellen E. Lee ◽  
Baichun Hou ◽  
Ipsit V. Vahia ◽  
Dilip V. Jeste
Keyword(s):  
Risk Factors ◽  
Differential Diagnosis ◽  
Life Events ◽  
Genetic Risk ◽  
Psychiatric Symptoms ◽  
Late Onset ◽  
Sociodemographic Factors ◽  
Sensory Loss ◽  
Adverse Life Events

Late-onset schizophrenia remains an understudied subtype of schizophrenia, despite growing recognition of its impact and distinction from early-onset schizophrenia. This chapter reviews the existing literature on late-onset schizophrenia including beginning with the nomenclature and epidemiology. Then we provide a review of key risk factors and correlates—including genetic risk, sex differences, comorbid sensory loss and physical illness, cognitive and psychiatric symptoms, sociodemographic factors, adverse life events, neuropathology, and inflammation. The chapter ends with clinical issues, including symptoms, differential diagnosis, treatments, and prognosis. Recent studies have examined the role of oestrogen treatments and a new therapy for tardive dyskinesia therapy as well as inflammatory mechanisms in schizophrenia.

scholarly journals A Case of Psychosis Due to Acute Hypocalcemia From Hypoparathyroidism

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A172-A173
Author(s):  
Joseph Theressa Nehu Parimi ◽  
John Chen Liu ◽  
Rajani Gundluru ◽  
Sowjanya Naha ◽  
Timur Gusov ◽  
...  
Keyword(s):  
Psychiatric Symptoms ◽  
Case Reports ◽  
Severe Depression ◽  
Altered Mental Status ◽  
Auditory Hallucinations ◽  
Psychotic Symptoms ◽  
Organic Psychosis ◽  
Neuropsychiatric Manifestations ◽  
History Of ◽  
Gait Abnormalities

Abstract A 61-year-old female with past medical history of depression, hypoparathyroidism (hypoPtH), and hypothyroidism had disappeared from her home and was found wandering a few hours away with persecutory delusions, visual and auditory hallucinations. Serum calcium (Ca) was 6.3 mg/dL (range 8.6–10.2), albumin 3.7 g/dL (range 3.5–5.2) and ionized Ca 0.89 mmol/L (range 1.12–1.30). She was admitted and treated with Ca and calcitriol. Work-up for altered mental status was negative except for hypocalcemia (hypoCa) and scattered bilateral basal ganglia calcifications (BGC) with cortical and subcortical frontal lobe calcifications on CT. Psychiatry diagnosed delirium due to hypoCa. Acute psychosis resolved once Ca levels improved. Diagnosis of idiopathic hypoPtH was in 1997. Her regimen included Ca citrate 1500mg daily and 10 mcg of Forteo twice daily. She had skipped her medications for at least 2 days prior to presentation. Her medical records revealed that she was seen for severe depression, progressive gait abnormalities, slowed movements, and imbalance, in 2015. CT scan and MRI brain showed BGC. Her son gave a history of multiple admissions for psychosis, violence, delusions with agitation, and wandering at times when the patient was hypoCa, which was diagnosed as schizophrenia. Neuropsychiatric disturbances are commonly associated with hypercalcemia. Review of literature found a few case reports of psychosis and hypoPtH 1,2 BGC is common in hypoPtH. Psychotic symptoms due to BGC include auditory hallucinations, delusions of influence, paranoid states, and complex perceptual distortions.3,5 HypoCa is associated with cognitive impairment. Neurological manifestations tend to improve with Ca correction, but psychiatric symptoms do not improve substantially.4,5 Further studies are needed in hypoPtH with BGC to appropriately diagnose organic psychosis. This is important in management of the vicious cycle of psychiatric illness leading to noncompliance resulting in psychosis. Prevention of BGC will play a key role. References: 1. Finan M, Axelband J. This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism. Am J Emerg Med. 2014;32:945.e1-4. 2. Ang AW, Ko SM, Tan CH. Calcium, magnesium, and psychotic symptoms in a girl with idiopathic hypoparathyroidism. Psychosom Med. 1995;57:299–302. 3. Burns K, Brodaty H. Fahr’s disease and psychosis. In: Sachdev PS, Keshavan MS, editors. Secondary schizophrenia. Cambridge: Cambridge University; 2010. p. 358–66. 4. Maiti A, Chatterjee S. Neuropsychiatric manifestations and their outcomes in chronic hypocalcaemia. J Indian Med Assoc. 2013;111:174–7. 5. Amara A, Novais C, Coelho M, Silva A, Curral R, Brandao I, Torres A. Organic psychosis due to hypoparathyroidism in an older adult: a case report. Braz. J. Psychiatry; 2016; 38(4)

Schizophrenia and familial idiopathic basal ganglia calcification: a case report

2001 ◽  
Vol 31 (4) ◽  
pp. 741-747 ◽  
Author(s):  
B. CHABOT ◽  
C. ROULLAND ◽  
S. DOLLFUS
Keyword(s):  
Case Report ◽  
Basal Ganglia ◽  
Computerized Tomography ◽  
Psychiatric Symptoms ◽  
Psychotic Symptoms ◽  
Basal Ganglia Calcification ◽  
First Degree Relatives ◽  
Idiopathic Basal Ganglia Calcification ◽  
The Subject ◽  
The Relationship

Background. Familial idiopathic basal ganglia calcification (FIBGC) is generally associated with neurological and psychiatric symptoms. An association between FIBGC and schizophrenia has been described but it remains uncertain. We studied the relationship between the presence and extent of basal ganglia calcification and schizophrenia in a multiply affected family.Method. Symmetrical basal ganglia calcifications (BGC) were detected on computerized tomography (CT) in a schizophrenic proband and led us to carry out CTs and standardized psychiatric evaluations (SADS – Endicott & Spitzer, 1978) in all available first-degree relatives (mother and six siblings).Results. Five subjects had BGC, including three subjects diagnosed as schizophrenic. Three subjects had no BGC and none of them was diagnosed as schizophrenic. We subdivided the BGC into three groups: massive (pallidum, striatum and dentate nuclei affected); medium (pallidum and striatum); and mild (pallidum only). The two subjects with massive BGC and one of the two with medium BGC had schizophrenia. The subject with mild BGC had no psychotic symptoms.Conclusion. Our results are consistent with the hypothesis that BGC favours the occurrence of a schizophrenia-like syndrome and that the risk of occurrence of this syndrome is proportional to the extent of calcification. These findings support the hypothesis that schizophrenia is determined by a disruption of thalamo–cortico–striatal circuits.

Basal ganglia calcification and psychosis in 22q11.2 deletion syndrome

2005 ◽  
Vol 20 (8) ◽  
pp. 567-569 ◽  
Author(s):  
M. Sieberer ◽  
H. Haltenhof ◽  
B. Haubitz ◽  
B. Pabst ◽  
K. Miller ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Psychiatric Disorders ◽  
Psychiatric Symptoms ◽  
22Q11.2 Deletion Syndrome ◽  
Deletion Syndrome ◽  
Psychotic Symptoms ◽  
22Q11.2 Deletion ◽  
Basal Ganglia Calcification ◽  
Future Work

AbstractIntracerebral calcifications are a facultative symptom of hypoparathyreoidism in 22q11.2 deletion syndrome (22qDS). We describe a patient with 22qDS, basal ganglia calcification (BGC) and psychotic symptoms and discuss the etiological connection of BGC with psychiatric symptoms. Future work needs to determine the prevalence of BGC in 22qDS and psychiatric disorders.

scholarly journals Neuropsychiatric manifestations in patient with normal pressure hydrocephalus improved with therapeutic lumbar tapping

2019 ◽  
Vol 7 (5) ◽  
pp. 1979
Author(s):  
Kumari Padma ◽  
Chandini . ◽  
Siddharth Shetty A. ◽  
Safeekh A. T. ◽  
Raghavendra B. S.
Keyword(s):  
Normal Pressure Hydrocephalus ◽  
Psychiatric Symptoms ◽  
Late Onset ◽  
Normal Pressure ◽  
Communicating Hydrocephalus ◽  
Psychomotor Activity ◽  
Manic Symptoms ◽  
Normal Limits ◽  
Neuropsychiatric Manifestations ◽  
General Physical

Normal pressure hydrocephalus is a communicating hydrocephalus without evident obstruction of the normal pathway of CSF flow. Normal-pressure hydrocephalus is a common cause of reversible dementia and it can also present with various psychiatric symptoms. A 76-year old man was brought to psychiatry OPD with history suggestive of decreased need for sleep for 8 days, disinhibited behaviour, increased libido, increased activity and increased talk for 4 days. On examination patient was noticed to be having increased psychomotor activity with increased talk, mood reported to be happy with elated affect, no content or perceptual disturbances were elicited. Cognitive functions were within normal limits. Personal and social judgement was impaired with grade 0 insight. General physical and systematic examinations were within normal limits. MRI reports showed ventricular enlargement suggestive of normal pressure hydrocephalus. Patient underwent diagnostic and therapeutic lumbar tapping. There was significant improvement in patient’s behavioural symptoms following therapeutic lumbar tapping. Therapeutic lumbar tapping in this case of normal pressure hydrocephalus was effective in the management of manic symptoms. Early identification of organic cause in late onset psychiatric disorders is necessary. Prompt intervention of the organic cause was effective in the management of manic symptoms.

Clinical overlap between behavioral variant of frontotemporal dementia and bipolar disorder: A case report

2016 ◽  
Vol 33 (S1) ◽  
pp. S335-S336 ◽  
Author(s):  
P. Oliveira ◽  
C. Roque ◽  
V. Santos ◽  
N. Madeira
Keyword(s):  
Bipolar Disorder ◽  
Frontotemporal Dementia ◽  
Psychiatric Symptoms ◽  
Late Onset ◽  
Single Photon ◽  
Photon Emission ◽  
Interpersonal Behavior ◽  
Psychotic Symptoms ◽  
Emission Computed Tomography ◽  
Global Pattern

The behavioral variant of frontotemporal dementia (FTD) often begins with psychiatric symptoms, including changes in personal conduct and/or interpersonal behavior. Prior to developing cognitive impairment, differentiating FTD from primary psychiatric disorders might be challenging.This work presents a case of a manic episode with psychotic features in a 61-year-old man, whom personality changes and daily life difficulties arouse and persist after optimal management of the active manic and psychotic symptoms. Neuropsychological assessment detailed severe deficits among visuospatial and planning performances. Structural neuroimaging (CT-scan) primary revealed a global pattern of brain volume reduction. Severe perfusion deficits on frontal and both parietal lobes were shown on 99mTc-HMPAO single-photon emission computed tomography (SPECT). The hypothesis of probable FTD (behavioral variant) was established.The present case highlights how putative atypical and late-onset forms of bipolar disorder (BD) might instead progress to FTD. Several links are being advanced between the BD and FTD, for instance the close involvement of the C9ORF72 gene in a group of BD patients which progresses to dementia. These relations have actually been on focus recently. The field is however still relatively unexplored.Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals Acute Psychosis Associated with Subcortical Stroke: Comparison between Basal Ganglia and Mid-Brain Lesions

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Aaron McMurtray ◽  
Ben Tseng ◽  
Natalie Diaz ◽  
Julia Chung ◽  
Bijal Mehta ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Psychiatric Symptoms ◽  
Symptomatic Relief ◽  
Acute Onset ◽  
Brain Lesions ◽  
Psychotic Symptoms ◽  
History Of ◽  
The Brain ◽  
Brain Ischemic Stroke ◽  
New Onset

Acute onset of psychosis in an older or elderly individual without history of previous psychiatric disorders should prompt a thorough workup for neurologic causes of psychiatric symptoms. This report compares and contrasts clinical features of new onset of psychotic symptoms between two patients, one with an acute basal ganglia hemorrhagic stroke and another with an acute mid-brain ischemic stroke. Delusions and hallucinations due to basal ganglia lesions are theorized to develop as a result of frontal lobe dysfunction causing impairment of reality checking pathways in the brain, while visual hallucinations due to mid-brain lesions are theorized to develop due to dysregulation of inhibitory control of the ponto-geniculate-occipital system. Psychotic symptoms occurring due to stroke demonstrate varied clinical characteristics that depend on the location of the stroke within the brain. Treatment with antipsychotic medications may provide symptomatic relief.

Rabeprazole and Psychiatric Symptoms

2007 ◽  
Vol 41 (7-8) ◽  
pp. 1315-1317 ◽  
Author(s):  
Giovanni Polimeni ◽  
Paola Cutroneo ◽  
Adele Gallo ◽  
Salvatore Gallo ◽  
Edoardo Spina ◽  
...  
Keyword(s):  
Adverse Reaction ◽  
Adverse Reactions ◽  
Potential Role ◽  
Psychiatric Symptoms ◽  
Panic Attacks ◽  
Persistent Symptoms ◽  
Neuropsychiatric Manifestations ◽  
History Of ◽  
Anxiety Depression

Objective: To report the case of a patient who developed marked anxiety associated with episodes of panic attacks after starting rabeprazole therapy. Case Summary: An otherwise healthy 55-year-old woman was prescribed rabeprazole 20 mg/day administered in the morning tor persistent symptoms of dyspepsia. Ten days later, she presented with a 7 day history of marked anxiety associated with panic attacks, night terror (pavor nocturnus), episodic mental confusion, and attention deficit. Within 2 days of discontinuing rabeprazole, the patient recovered completely from the neuropsychiatric manifestations. Subsequent esomeprazole therapy did not cause psychiatric symptoms. Discussion: Rabeprazole-induced hypergastrinemia may have played a role in this neuropsychiatric adverse reaction. Several lines of evidence have indicated that gastrin-releasing peptide, whose release is mediated by proton pump inhibitor (PPI)–induced secretion of gastrin, is involved in regulating aspects of behavior that might be altered in disorders such as anxiety, depression, and dementia. The fact that rabeprazole has the highest capacity of inducing gastrin increase compared with other PPIs might explain why our patient's panic symptoms disappeared after switching to esomeprazole. Based on the Naranjo probability scale, rabeprazole was the probable cause of the adverse reaction. Conclusions: Specific studies are needed to investigate the potential role of PPI-induced hypergastrinemia in neuropsychiatrie adverse reactions.

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