Suspect Autoimmune or demyelinating disorder if..
1. Fatigue or cognitive impairment out of proportion to the mood symptoms or depression
2. Atypical presentation
3. Not responding to anti-depressants or anti-psychotics
4. Presence of EPS with minimal dose of typical anti-psychotics
-- To monitor BP and electrolytes if we suspect any autoimmune disorders
Neuropsychiatric manifestations of other infectious and Prion diseasesSravanthi Penubarthi
Detailed neurological examination is necessary in all patients of psychiatric illnesses , especially with more of atypical presentation or poor response to treatment , to rule out any of the infectious causes.
In case of patients with psychiatric illnesses, with more of focal neurological deficits, one should consider the probability of any CNS infection.
Patients with atypical presentation of Psychiatric disorder with neurocognitive abnormalities, aggressiveness, late onset with acute behavioral symptoms, and lack of previous history of psychiatric illness , there is a need to consider syphilis.
A diagnosis of CJD should be considered when an adult patient develops dementia rapidly and myoclonus.
This document discusses reversible causes of dementia and delirium. It begins by defining major neurocognitive disorder and reversible dementias. Common reversible causes of dementia include central nervous system infections, normal pressure hydrocephalus, nutritional deficiencies, drugs, endocrine disorders, depression, and sleep apnea. Delirium is then discussed, including risk factors, pathophysiology, clinical subtypes, DSM-5 criteria, assessment scales, differential diagnosis, course, prevention, and management. Reversible dementias are estimated to account for 8-40% of dementia cases. Early diagnosis and treatment of the underlying cause can improve cognitive functioning.
A 64-year-old woman presented with complaints of forgetfulness, difficulty cooking and managing household tasks, and inability to identify relatives over the past year. Neurological examination and investigations revealed no abnormalities except a low score on the Montreal cognitive assessment. This document defines dementia, discusses its causes and types, presents assessment tools and management strategies, and emphasizes the importance of a multidisciplinary approach and caregiver support.
Schizophrenia A chronic mental disorder involving a breakdown in the relation between thought, emotion, and behaviour, leading to faulty perception, inappropriate actions and feelings, withdrawal from reality and personal relationships into fantasy and delusion, and a sense of mental fragmentation.
Antipsychotic Agents Antipsychotic drugs are able to reduce psychotic symptoms in a wide variety of conditions, including schizophrenia, bipolar disorder, psychotic depression and drug induced psychosis. They have also been termed neuroleptics, because they suppress motor activity and emotionalityClinical Efficacy of Antipsychotic Drugs
Antipsychotic drugs are effective in controlling symptoms of acute schizophrenia, when large doses may be needed.
Long-term antipsychotic treatment is often effective in preventing recurrence of schizophrenic attacks, and is a major factor in allowing schizophrenic patients to lead normal lives.
Classification of Antipsychotic Drugs Typical antipsychotics Phenothiazines (Chlorpromazine, Perphenazine, Fluphenazine, Thioridazine) Thioxanthenes (Flupenthixol, Clopenthixol) Butyrophenones (Haloperidol, Droperidol)
Atypical antipsychotics (Clozapine, Risperidone, Sulpiride, Olanzapine, Aripiprazole)
Depot preparations are often used for maintenance therapy.
Approximately 40% of chronic schizophrenic patients are poorly controlled by antipsychotic drugs; clozapine may be effective in some of these ‘antipsychotic-resistant’ cases.
a syndrome of persistent widespread pain, stiffness, fatigue, disrupted and unrefreshing sleep, and cognitive difficulties, often accompanied by multiple other unexplained symptoms, and functional impairment of activities of daily living.
Pharmacology I, Antipsychotic (Neuroleptic) Drugs NK-Trimmed.pptxAhmad Kharousheh
This document summarizes antipsychotic drugs used to treat psychosis and schizophrenia. It discusses the dopamine hypothesis for the pathophysiology of schizophrenia and how first-generation "typical" antipsychotics work by blocking dopamine D2 receptors, which can cause extrapyramidal side effects. Second-generation "atypical" antipsychotics have a lower risk of these side effects by also blocking serotonin receptors. Clozapine is reserved for treatment-resistant cases. Long term use of antipsychotics can cause neurological side effects like tardive dyskinesia. The document outlines the mechanisms of action, therapeutic uses, and adverse effects of antipsychotic drugs.
Schizophrenia is a disease that affects thoughts, emotions, and actions. It was first described in the 19th century and given its current name in 1911. There are various biological, psychological, and social factors involved in its etiology. Genetics plays a major role, with risk increasing if a family member has schizophrenia. Symptoms include positive symptoms like delusions and hallucinations as well as negative symptoms such as apathy. It is diagnosed based on symptoms and differential diagnosis is needed to rule out other conditions. Outcomes vary but many experience impairment. Management involves antipsychotic medication, psychosocial support, and addressing any substance abuse or medical issues.
Organic psychosis can be caused by structural brain lesions or physiological dysfunction. Herpes simplex encephalitis is a rare but potential organic cause of psychosis, typically presenting with fever, headache, hallucinations and altered mental status. While rare, herpes encephalitis can trigger anti-NMDA receptor encephalitis months later. Viral infections during development may increase schizophrenia risk later in life via immune-mediated brain damage. Infections can also cause chronic neuropsychiatric symptoms if the virus persists dormantly or actively in the brain. Organic causes of psychosis should be considered if symptoms are atypical of functional disorders or if a medical condition affects the nervous system.
Neuropsychiatric manifestations of other infectious and Prion diseasesSravanthi Penubarthi
Detailed neurological examination is necessary in all patients of psychiatric illnesses , especially with more of atypical presentation or poor response to treatment , to rule out any of the infectious causes.
In case of patients with psychiatric illnesses, with more of focal neurological deficits, one should consider the probability of any CNS infection.
Patients with atypical presentation of Psychiatric disorder with neurocognitive abnormalities, aggressiveness, late onset with acute behavioral symptoms, and lack of previous history of psychiatric illness , there is a need to consider syphilis.
A diagnosis of CJD should be considered when an adult patient develops dementia rapidly and myoclonus.
This document discusses reversible causes of dementia and delirium. It begins by defining major neurocognitive disorder and reversible dementias. Common reversible causes of dementia include central nervous system infections, normal pressure hydrocephalus, nutritional deficiencies, drugs, endocrine disorders, depression, and sleep apnea. Delirium is then discussed, including risk factors, pathophysiology, clinical subtypes, DSM-5 criteria, assessment scales, differential diagnosis, course, prevention, and management. Reversible dementias are estimated to account for 8-40% of dementia cases. Early diagnosis and treatment of the underlying cause can improve cognitive functioning.
A 64-year-old woman presented with complaints of forgetfulness, difficulty cooking and managing household tasks, and inability to identify relatives over the past year. Neurological examination and investigations revealed no abnormalities except a low score on the Montreal cognitive assessment. This document defines dementia, discusses its causes and types, presents assessment tools and management strategies, and emphasizes the importance of a multidisciplinary approach and caregiver support.
Schizophrenia A chronic mental disorder involving a breakdown in the relation between thought, emotion, and behaviour, leading to faulty perception, inappropriate actions and feelings, withdrawal from reality and personal relationships into fantasy and delusion, and a sense of mental fragmentation.
Antipsychotic Agents Antipsychotic drugs are able to reduce psychotic symptoms in a wide variety of conditions, including schizophrenia, bipolar disorder, psychotic depression and drug induced psychosis. They have also been termed neuroleptics, because they suppress motor activity and emotionalityClinical Efficacy of Antipsychotic Drugs
Antipsychotic drugs are effective in controlling symptoms of acute schizophrenia, when large doses may be needed.
Long-term antipsychotic treatment is often effective in preventing recurrence of schizophrenic attacks, and is a major factor in allowing schizophrenic patients to lead normal lives.
Classification of Antipsychotic Drugs Typical antipsychotics Phenothiazines (Chlorpromazine, Perphenazine, Fluphenazine, Thioridazine) Thioxanthenes (Flupenthixol, Clopenthixol) Butyrophenones (Haloperidol, Droperidol)
Atypical antipsychotics (Clozapine, Risperidone, Sulpiride, Olanzapine, Aripiprazole)
Depot preparations are often used for maintenance therapy.
Approximately 40% of chronic schizophrenic patients are poorly controlled by antipsychotic drugs; clozapine may be effective in some of these ‘antipsychotic-resistant’ cases.
a syndrome of persistent widespread pain, stiffness, fatigue, disrupted and unrefreshing sleep, and cognitive difficulties, often accompanied by multiple other unexplained symptoms, and functional impairment of activities of daily living.
Pharmacology I, Antipsychotic (Neuroleptic) Drugs NK-Trimmed.pptxAhmad Kharousheh
This document summarizes antipsychotic drugs used to treat psychosis and schizophrenia. It discusses the dopamine hypothesis for the pathophysiology of schizophrenia and how first-generation "typical" antipsychotics work by blocking dopamine D2 receptors, which can cause extrapyramidal side effects. Second-generation "atypical" antipsychotics have a lower risk of these side effects by also blocking serotonin receptors. Clozapine is reserved for treatment-resistant cases. Long term use of antipsychotics can cause neurological side effects like tardive dyskinesia. The document outlines the mechanisms of action, therapeutic uses, and adverse effects of antipsychotic drugs.
Schizophrenia is a disease that affects thoughts, emotions, and actions. It was first described in the 19th century and given its current name in 1911. There are various biological, psychological, and social factors involved in its etiology. Genetics plays a major role, with risk increasing if a family member has schizophrenia. Symptoms include positive symptoms like delusions and hallucinations as well as negative symptoms such as apathy. It is diagnosed based on symptoms and differential diagnosis is needed to rule out other conditions. Outcomes vary but many experience impairment. Management involves antipsychotic medication, psychosocial support, and addressing any substance abuse or medical issues.
Organic psychosis can be caused by structural brain lesions or physiological dysfunction. Herpes simplex encephalitis is a rare but potential organic cause of psychosis, typically presenting with fever, headache, hallucinations and altered mental status. While rare, herpes encephalitis can trigger anti-NMDA receptor encephalitis months later. Viral infections during development may increase schizophrenia risk later in life via immune-mediated brain damage. Infections can also cause chronic neuropsychiatric symptoms if the virus persists dormantly or actively in the brain. Organic causes of psychosis should be considered if symptoms are atypical of functional disorders or if a medical condition affects the nervous system.
The recognition of bipolar disorder in primary careNick Stafford
Bipolar disorder and the complexities of screening and diagnosis in primary care. How more accurate detection and an integrated care pathway with secondary care can improve the diagnosis and outcome of the treatment of the disorder.
a presentation on autoimmune encephalitis, paraneoplastic syndrome. their types and various imaging and lab finding
their differential diagnosis
acute and long term management plans
Late onset mania is a kind of Psychiatric illness in which Manic symptoms develops for the first time after the age of 60 years or the continuation of recurrent bipolar illness.
1) Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. The main pathologies are amyloid plaques and neurofibrillary tangles in the brain.
2) Current treatments only temporarily slow the worsening of symptoms but do not stop or reverse the disease process. Cholinesterase inhibitors and memantine are used to manage cognitive and behavioral symptoms.
3) The FDA recently approved aducanumab as the first drug that targets and reduces amyloid plaques in the brain, which may slow clinical decline in Alzheimer's disease.
Dementia, by Dr Kamal Kejriwal MD AAFP, CMD Geriatric Fellowship Program Director, Kaiser Fontana
Dementia, by Dr Sherif Iskander Geriatric Fellows Dr Marian Assal, Geriatrician, Kaiser Fontana, as presented within the 2018 January GWEP conference
This document presents a case study of a 28-year-old male patient admitted to the psychiatric ward for severe alcohol withdrawal symptoms including hallucinations and delusions occurring 5 days after his last drink. The patient has a 6-year history of heavy alcohol use and family history of alcoholism. He is diagnosed with alcohol withdrawal delirium based on his symptoms and history. His treatment plan includes benzodiazepines and antipsychotics to relieve his symptoms. Over 4 days of treatment his symptoms improve and he is discharged in a better condition.
The document describes a case of delirium in an 81-year-old man. He presented with fever, confusion, and urinary retention and was diagnosed with a urinary tract infection. His risk factors for delirium included older age, hypertension, smoking, and acute infection. Non-pharmacological management includes ensuring nutrition, safety precautions, and early rehabilitation. Atypical antipsychotics in low doses may help control symptoms, though the prognosis depends on resolving the underlying medical issues. Preventing delirium requires a multidisciplinary approach and addressing reversible risk factors.
(1) This document discusses neuroinflammatory disorders like multiple sclerosis and neuromyelitis optica. MS most commonly affects women aged 15-45 and has a relapsing-remitting clinical course. (2) It also summarizes evaluation, treatment including immunotherapies, and guidelines for vaccination in MS patients. (3) Autoimmune encephalitis can be paraneoplastic or associated with antibodies like NMDA receptor antibodies, and may respond to immunotherapy and tumor treatment.
The document summarizes information about depression and schizophrenia. It discusses definitions, types, etiology, signs and symptoms, pathophysiology, diagnosis, and complications for each condition. Depression is characterized by depressed mood and loss of interest, while schizophrenia involves disorganized thinking, delusions, and hallucinations. Both conditions have genetic and environmental risk factors and can be diagnosed based on clinical criteria involving symptoms. Complications can include issues like stigma, drug interactions, and poor physical health.
A 38-year-old man presented with seizures and was diagnosed with cortical venous thrombosis. He had multiple risk factors including diabetes, hyperhomocysteinemia, and dyslipidemia. He was treated with anticoagulation but continued having seizures. Imaging later revealed a venous infarct. His symptoms gradually improved with treatment but he was discharged with some residual neurological deficits. Cortical venous thrombosis can be challenging to diagnose but outcomes have improved with prompt diagnosis and treatment. Hyperhomocysteinemia is an increasingly recognized risk factor.
Module: Pharmacotherapy III
Module Coordinator: Dr. Arwa M. Amin Mostafa
Academic Level: Postgraduate, Master of Pharmacy in Clinical Pharmacy
School: Dubai Pharmacy College
Year of first presented in Class: 2018
This presentation is for Educational purpose. It has no commercial value associated with it.
Schizophrenia is a complex psychiatric disorder characterized by disorganized thoughts, delusions, hallucinations, inappropriate affect, and impaired social functioning. The exact causes are unknown but likely involve genetic, brain chemical, environmental, and family history factors. Brain imaging shows enlarged ventricles and decreased cortical size, particularly in the left temporal lobe. Symptoms include positive symptoms like hallucinations, negative symptoms like loss of interest, and mood symptoms. Treatment involves pharmacological therapy with antipsychotics and non-pharmacological approaches like therapy, social skills training, and vocational rehabilitation.
This document discusses several common neurological disorders seen in patients with HIV/AIDS, including toxoplasmosis, herpes simplex virus encephalitis, cytomegalovirus encephalitis, cryptococcal meningitis, dementia, primary CNS lymphoma, and progressive multifocal leukoencephalopathy. For each disorder, it covers causes, frequency, presentation, diagnosis, and treatment approaches. The overall purpose is to educate participants on identifying, diagnosing, and managing neurological complications in HIV/AIDS patients.
Delirium is characterized by an acute decline in awareness and cognition, particularly attention. It is a medical emergency caused by reversible brain dysfunction. The document discusses the risk factors, causes, manifestations, diagnosis and treatment of delirium. Precipitating factors include medical illnesses, surgery, medications and the hospital environment. Treatment involves identifying and treating the underlying medical cause, minimizing medications, and preventing complications through early mobilization and cognitive stimulation.
Schizophrenia is a chronic psychiatric disorder that affects around 1% of the population. It causes distortions in thinking, perception, emotions, language, sense of self and behavior. Common symptoms include hallucinations, delusions, disorganized speech and behavior. Treatment involves antipsychotic medications to manage symptoms as well as psychosocial therapies to support independent living. Nursing care focuses on ensuring patient safety, promoting treatment adherence, and helping patients maintain functioning.
This document discusses several types of psychopathology including schizophrenia, mood disorders like depression, and anxiety disorders. It provides information on the symptoms, potential causes like genetic and environmental factors, and treatments for each type of disorder. For schizophrenia, it discusses brain changes and the dopamine hypothesis as well as historical and modern drug treatments. For depression, it covers brain changes, therapies like ECT and TMS, and theories about serotonin. Anxiety disorders covered include phobias, panic disorder, PTSD, OCD, and Tourette's syndrome.
This document provides information about Multiple Sclerosis (MS). It defines MS as a chronic neurological disorder that affects the central nervous system, where myelin is destroyed in the brain and spinal cord, causing scarring in multiple sites. MS is the most common disabling condition in young adults. While its cause is unknown, it involves an immunological reaction destroying myelin. Symptoms vary between patients and can include vision changes, numbness, weakness, and problems with coordination or bladder control. Diagnosis involves MRI imaging and other tests. Currently, there is no cure for MS but treatments can help reduce symptoms and slow progression.
covering the topic of chronic immune mediated demyelinating neuropathies with a detailed focus on the typical form of chronic inflammatory demyelinating polyradiculoneuropathy (Typical CIDP).
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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a presentation on autoimmune encephalitis, paraneoplastic syndrome. their types and various imaging and lab finding
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acute and long term management plans
Late onset mania is a kind of Psychiatric illness in which Manic symptoms develops for the first time after the age of 60 years or the continuation of recurrent bipolar illness.
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This document presents a case study of a 28-year-old male patient admitted to the psychiatric ward for severe alcohol withdrawal symptoms including hallucinations and delusions occurring 5 days after his last drink. The patient has a 6-year history of heavy alcohol use and family history of alcoholism. He is diagnosed with alcohol withdrawal delirium based on his symptoms and history. His treatment plan includes benzodiazepines and antipsychotics to relieve his symptoms. Over 4 days of treatment his symptoms improve and he is discharged in a better condition.
The document describes a case of delirium in an 81-year-old man. He presented with fever, confusion, and urinary retention and was diagnosed with a urinary tract infection. His risk factors for delirium included older age, hypertension, smoking, and acute infection. Non-pharmacological management includes ensuring nutrition, safety precautions, and early rehabilitation. Atypical antipsychotics in low doses may help control symptoms, though the prognosis depends on resolving the underlying medical issues. Preventing delirium requires a multidisciplinary approach and addressing reversible risk factors.
(1) This document discusses neuroinflammatory disorders like multiple sclerosis and neuromyelitis optica. MS most commonly affects women aged 15-45 and has a relapsing-remitting clinical course. (2) It also summarizes evaluation, treatment including immunotherapies, and guidelines for vaccination in MS patients. (3) Autoimmune encephalitis can be paraneoplastic or associated with antibodies like NMDA receptor antibodies, and may respond to immunotherapy and tumor treatment.
The document summarizes information about depression and schizophrenia. It discusses definitions, types, etiology, signs and symptoms, pathophysiology, diagnosis, and complications for each condition. Depression is characterized by depressed mood and loss of interest, while schizophrenia involves disorganized thinking, delusions, and hallucinations. Both conditions have genetic and environmental risk factors and can be diagnosed based on clinical criteria involving symptoms. Complications can include issues like stigma, drug interactions, and poor physical health.
A 38-year-old man presented with seizures and was diagnosed with cortical venous thrombosis. He had multiple risk factors including diabetes, hyperhomocysteinemia, and dyslipidemia. He was treated with anticoagulation but continued having seizures. Imaging later revealed a venous infarct. His symptoms gradually improved with treatment but he was discharged with some residual neurological deficits. Cortical venous thrombosis can be challenging to diagnose but outcomes have improved with prompt diagnosis and treatment. Hyperhomocysteinemia is an increasingly recognized risk factor.
Module: Pharmacotherapy III
Module Coordinator: Dr. Arwa M. Amin Mostafa
Academic Level: Postgraduate, Master of Pharmacy in Clinical Pharmacy
School: Dubai Pharmacy College
Year of first presented in Class: 2018
This presentation is for Educational purpose. It has no commercial value associated with it.
Schizophrenia is a complex psychiatric disorder characterized by disorganized thoughts, delusions, hallucinations, inappropriate affect, and impaired social functioning. The exact causes are unknown but likely involve genetic, brain chemical, environmental, and family history factors. Brain imaging shows enlarged ventricles and decreased cortical size, particularly in the left temporal lobe. Symptoms include positive symptoms like hallucinations, negative symptoms like loss of interest, and mood symptoms. Treatment involves pharmacological therapy with antipsychotics and non-pharmacological approaches like therapy, social skills training, and vocational rehabilitation.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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4. INTRODUCTION
•An autoimmune disease is an illness that causes the immune
system to produce antibodies that attack normal body
tissues.1
•In 1895, William Osler , for the first time, gave the description
of an autoimmune disease affecting the brain (psychosis in
SLE) 2
•The production of auto antibodies against neuronal antigens
can interfere with synaptic transmission causing direct
neuronal injury. 3
CHRI, 2018 4
6. NEURO-PSYCHIATRIC MANIFESTATIONS
Neuro-psychiatric manifestations vary in severity and symptomatology
based on the organ involved.
The most common psychiatric manifestations:
•Progressive cognitive dysfunction
•Emotional instability
•Sleep disorders
•Depersonalization and derealization
•Depression
•Anxiety
•Psychotic symptoms (referential delusions and hallucinations)
CHRI, 2018 6
7. • A 16-year old girl was brought to ER with 7days history of gradual
progression of
o headache, body ache & loss of appetite
o excessive talking, muttering, tearfulness and irritability
o withdrawn and non-communicative.
• On examination, waxy flexibility, negativism, and immobility were found.
• Diagnosed as Acute psychosis with catatonic features and treated with
lorazepam 4-6mg/day and Risperidone 2-4 mg/day. Due to slow
improvement, 6 ECTs were given.
• Patient worsened after moderate improvement and a facial butterfly rash
developed.
• Patient was subjected to LE Cell test and Anti-DS DNA test, both of which
were positive.
CASE VIGNETTE – 14
CHRI, 2018 7
8. CASE VIGNETTE -2 5
41 year Man presented to Psychiatric OPD with
Depressive symptoms for 2 months with complaints of hearing his
deceased wife’s voice in the house occasionally.
Started on psychotherapy sessions (twice monthly) and 20mg of
fluoxetine daily.
After 2 weeks , reported no improvement in symptoms and complained
of death wishes , however no suicidal ideas – Continued Fluoxetine and
Psychotherapy once weekly sessions – lost to followup.
Four months later, presented to ER with delirium, mild fever, and visual
and auditory hallucinations with examination and lab findings of weak,
thready pulse, severe hypotension (70 systolic), and severe hyponatremia
and hyperkalemia.
Diagnosed as ADDISONIAN CRISIS and treated in ICU .
CHRI, 2018 8
9. SLE
• Chronic disease that causes
inflammation in connective
tissues which provide flexibility
to body structures.
• Skin changes are frequent, with
classical butterfly eruption over
nose and cheeks.
• With early detection and
effective treatment with
steroids, it mostly may present
as recurrent mild illness with
prolonged asymptomatic CHRI, 2018 9
11. NEUROPSYCHIATRIC
MANIFESTATIONS 6,7
Can be the earliest manifestations
of SLE.
In up to 40% , seen during the
first year of SLE diagnosis.
Can occur independently of active
systemic disease and without
serologic activity.
Prevalence of NPSLE
• 14% - 80% in adults
• 22% - 95% in children
Cognitive impairment (20-80%)
Depression (65%)
Anxiety(40%)
Psychosis (2-11%)
Delirium(1-7%)
CHRI, 2018 11
12. COGNITIVE IMPAIRMENT & SLE
Seen in 75% patients with NPSLE
Generally Mild , often transient
Components affected
Attention and concentration
Memory and processing speed
Executive and visuospatial problems.
Greater cognitive impairment seen in those with steroid use or
comorbid depression.
Degree of impairment is associated with severity of illness
CHRI, 2018 12
13. DEPRESSION & SLE
In patients with depression in SLE , symptoms commonly seen
are
•Fatigue
•Reduced muscle strength
•Sleep disturbance
•Pain
CHRI, 2018 13
16. DELIRIUM & SLE
• Initially considered as most frequent (30%) complain
associated with SLE
• Currently seen only in 3% of patients with SLE
• LUPUS PSYCHOSIS – hours to days and completely subside
• Symptoms can be
• Mild confusion with clouding of consciousness
• More florid symptoms with visual and auditory
hallucinations CHRI, 2018 16
17. TREATMENT FOR NPSLE 10
Mild NPSLE – symptomatic treatment
New onset NPSLE or severe symptoms Immunosuppressant or
other therapy directed against autoimmunity.
Systemic gluco-corticoids show response in 60-75% patients.
Cyclophosphamide is the most common drug used for NPSLE.
11
Severe cases - addition of plasmapharesis as an adjuvant to
steroids or cyclophosphamide.
Rituximab (anti CD-20 monoclonal antibody) – refractory
NPSLE
CHRI, 2018 17
18. ANTI-NMDA
RECEPTOR
ENCEPHALITIS
• Initially, thought to be a
paraneoplastic disorder, occurring
in young females in association
with an ovarian teratoma .
• Later research suggested that It
can occur with or without a tumor,
and can arise in children and
young adults, both male and
female.
• Prevalence – around 1 % in ICU
admitted individuals of 18-
35years age group 11
DORSOLATERA
L PREFRONTAL
CORTEX
CHRI, 2018 18
19. 75 % pts present with psychiatric illness
Diagnosed with Acute psychosis / Mania with or
without psychotic symptoms/Drug abuse/
malingering
Treated with anti-psychotic
Mostly develop Features suggestive of NMS
On detailed Neurological examination and further
investigations
Diagnosed as ANTI-NMDA RECEPTOR ENCEPHALITIS
CHRI, 2018 19
24. TREATMENT FOR PSYCHIATRIC
SYMPTOMS 12,14
Quetiapine as the initial drug for psychotic symptoms and
agitation
Anti-cholinergics
Benzodiazepines to manage sleep
Trazadone
Clonidine
Acutely agitated or psychotic patients who refuse medications
often respond well to Chlorpromazine.
ECT has also shown to be a safe and effective option
(particularly in catatonia)
CHRI, 2018 24
25. PSORIASIS Genetically primed
individuals
Unmyelinated
terminals of sensory
fibers in skin
Substance P & other
Neuropeptides
Local neurogenic
Inflammation
• Persistent skin disease
that causes rapid
turnover of skin cells
forming thick silvery
scales, itchy, dry and
red patches.
• Incidence – 1-2%
• Bimodal distribution
with early onset in
females.
NEUROGENIC INFLAMMATION HYPOTHESIS
OF PSORIASIS (FARBER Et.al) 15
CHRI, 2018 25
26. Most prevalent Psychiatric
manifestations associated with
psoriasis 16
• Sexual disorders (71%)
• Sleep disorders (50%)
• Depression
• Anxiety
Others include :
• Substance dependence or abuse
• somatoform disorders
• Schizophrenia/other psychoses
• Bipolar disorder
• Eating disorders
Psoriasis
Social stigma
Low self-
esteem
Poor
psychosocial
adjustment
Poor coping
mechanism
Worsen
other
Physical
conditions
CHRI, 2018 26
27. DEPRESSION & PSORIASIS
17,18
• High concentrations of
substance P
• Defect in β-adrenergic
function
• Low melatonin
secretion
• Raised pro-
inflammatory cytokines
CHRI, 2018 27
28. POSSIBLE ETIOLOGICAL FACTORS 16
SEXUAL DISORDERS SLEEP DISORDERS 20
Low self-esteem and
psychological factors
Depression
Pruritus Pain due to skin lesions
Psoriatic arthritis Obstructive sleep Apnea
Side-effects of psoriasis
treatment
Pruritus
Other psychiatric comorbidities Psoriatic Arthritis / Joint pain
Common symptoms seen
Decreased sexual desire
Anorgasmia
Erectile dysfunction
Early morning awakening
Increase in nocturnal awakening
Daytime sleepiness
CHRI, 2018 28
29. RHEUMATOID
ARTHRITIS
• More in women.
• 4-5th decade of life.
• Affects joints leading to
permanent deformations
• May present also with extra-
articular manifestations and
systemic complications
CHRI, 2018 29
30. Approximately one-fifth of patients with RA have a psychiatric
disorder and a similar number have subsyndromal psychiatric
symptoms. 21
Neuropsychiatric manifestations in RA can arise through any of the
following four processes 21
1. Direct CNS involvement
2. Secondary effects of the illness or its treatments
3. Emotional reactions to chronic illness
4. Comorbid primary psychiatric illness.
It is seen that, in most cases , psychiatric symptoms are due to
emotional reactions to having a painful potentially disabling and
immobilizing chronic illness adversely affecting work, family, social life,
and leisure activity. 22
CHRI, 2018 30
31. The frequency of depression and anxiety disorders among
patients with RA ranges from 14 - 42%. 22
Among female patients with RA who committed suicide, 90% had
a depressive disorder. 23
It was reported that RA Patients with depression complain
significantly higher levels of pain, greater number of painful joints,
and poorer functional ability
The main psychosocial factors, that cause negative adaptation are
include exposure to stressors , sleep disturbance , premorbid
anxiety.
Rarely they can manifest with dissociative disorders or psychotic
symptoms.
CHRI, 2018 31
32. ADDISON’S
DISEASE7
• Medical condition
characterized by chronic
adrenal insufficiency leading
to failure of glucocorticoid
secretion.
• 6-110 cases diagnosed per
100,000 in the world per year.
• Usually effects 30-50 year age
group. CHRI, 2018 32
33. EEG
Abnormality
•Bursts of 3-6sec of high voltage potentials with no definite cortical focus
•M/c - Diffuse slowing
Glucocorticoid
Deficiency
•Normally, cortisol binds to GC receptor in brain , modifying the gene transcription
•Deficiency causes memory impairment & cognitive changes and causes Neuroexcitability leading to enhanced ability
to detect sensory input (high tendency to develop hallucinations)
Increased
Endorphins
•POMC – rises ACTH and endorphin release.
•Elevated CSF endorphins – associated with Psychosis
Metabolic
Changes
•Hypoxia secondary to Hypotension – Changes in MSE
•Severe Hypoglycemia – Cogitive changes & coma
•Hyponatremia – Encephalopathy & brain damage
ETIOPATHOGENESIS 24
CHRI, 2018 33
34. NEUROPSYCHIATRIC MANIFESTATIONS
25
Seen in 64-84% of affected
individuals.
Common presentation -
•Depression
•Sleep disturbance
•lack of motivation
•Anxiety
•Agitation
•Memory impairment
Rare manifestations:
• Psychosis
• Self-mutiliation
• Severe cognitive disturbances
CHRI, 2018 34
35. MYASTHENIA
GRAVIS
• Chronic, autoimmune disease
caused by anti-cholinergic
antibodies that target
neuromuscular junctions
• Prevalence of about 20 per
1,00,000
• Unrecognized initially because
the psychiatric symptoms may
coincide with those of the actual
disease. CHRI, 2018 35
36. NEUROPSYCHIATRIC
MANIFESTATIONS 26
•20% patients – psychiatric symptoms
are the primary presentation
•40-50% patients experience
comorbid psychiatric illnesses.
•Depression & Adjustment disorders –
Most common
•Others- Insomnia; Memory
disturbances; Anxiety disorders;
Suicidality.
SLEEP DISORDERS 27
•Shorter REM sleep duration
•Increased number of
awakenings
•Reduced quality of sleep
•Increased dream recall
•Shallow Sleep EEG
MEMORY DISTURBANCES 28
•Poor performance in
•delayed recall memory
•verbal learning tests.
CHRI, 2018 36
37. ANTI-PHOSPHOLIPID SYNDROME
7,29
Similar to SLE
Primary APS – Most common acquired thrombophilia
The most common psychiatric symptom is cognitive impairment.
Usually associated with the presence of vascular lesions in
white matter and are difficult to differentiate in MRI from
demyelination lesions seen in multiple sclerosis.
May coexist with characteristic skin lesions called “livedo
reticularis”.
Other Psychiatric manifestations include – Depression ; Agression
and mania
CHRI, 2018 37
38. Sjogrens
Syndrome
•Mimic MS
•Anxiety(48%)
•Depression (32%)
Systemic sclerosis
•Neuropsychiatric
symptoms are
rare.
•Most common-
Depression (due
to chronic
illness)
Other
Autoimmune
•Type-1 DM
•Hashimoto’s
thyroiditis
OTHER AUTOIMMUNE DISORDERS
WITH PSYCHIATRIC MANIFESTATIONS 7,30
CHRI, 2018 38
39. •SSRI – preferred
•TCA and MAOI – to be cautious in
myasthenia & psoriasis
Antidepressa
nts
•Short acting BZDs are preferred
•Oxazepam ; lorazepam
Benzodiazepin
es
•Lithium – better
•Valproate & carbamazepine
Mood
Stabilizers
Anti-
psychotics
Haloperidol, amisulpride , Risperidone and
paliperidone – safer (To be monitored for EPS)
TREATMENT
CHRI, 2018 39
41. INTRODUCTION
Demyelinating disorders have a common pathology, i.e., the
partial or complete loss of the myelin sheath surrounding axons
in the white matter of brain and spinal cord 31
It is often secondary to an infectious, ischemic, metabolic, or
hereditary disorder or to a toxin/alcohol.
In primary demyelinating disorders, autoimmune mechanism is
suspected as the pathogenesis.
As these axons are present throughout the brain and spinal
cord, lesions may occur diffusely, resulting in complex and
widespread neurological and psychiatric symptoms32
CHRI, 2018 41
43. 27-year-old man with no prior psychiatric disorder or drug abuse was presented with 3
years history of
• Fear with the feeling of being followed by others, without any external stressor
• Hesitation and muttering, irritability, anger outbursts, bad tempering, and
antisocial behavior
• Thought his colleagues at work are likely to harm him due to his good skills at his
job.
• Depression, severe fatigue and loss of energy, loss of appetite, and weight loss
• Joint stiffness and loss of movement control at upper and lower limbs.
After 6 months from the appearance of symptoms, he was brought to a psychiatric office
being uncertain of hallucinogenic drug abuse.
The psychiatrist prescribed citalopram 20 mg OD, risperidone 2 mg TDS & Biperiden 2mg
TDS
After a month of medications , due to no improvement in symptoms , patient was
referred to carry out MRI to rule out organic disorders.
Gradually he developed paresthesia, upper and lower limb muscle weakness, ataxia, and
urinary incontinency.
The T2-weighted MRI demonstrated periventricular and white matter multiple sclerotic
CASE VIGNETTE - 3
33
CHRI, 2018 43
44. MULTIPLE SCLEROSIS 34
Definition Chronic inflammatory disease in the CNS with a
progressive demyelination of nerve cells & damage in
sensory-motor pathway that cause specific
neurological and psychological symptoms.
Prevalence 5-9/1lakh population (India)
More common Women ; 20-50 years age
Diagnosis Presence of 2 attacks, involving different parts of the
CNS, separated by a period of at least 1 month &
lasting a minimum of 24 hours.
Lab
investigations
• CSF – atleast 2 oligoclonal bands or raised IgG
synthesis
• Evoked potentials (VEP & SSEP) – slowed or absent
MRI • T2-hyperintense lesions and gadolinium-enhancing
CHRI, 2018 44
47. COGNITIVE IMPAIRMENT & MS
Seen in 50-70 % patients
Components affected are
• Memory
• Information processing
• Executive functioning
• Attention & concentration (occupational impairment)
Intellectual & language functioning – relatively intact.
Minimal Assessment of Cognitive Function in MS
(MACFIMS)35
CHRI, 2018 47
49. DEPRESSION & MS 36,37
Lifetime prevalence – 50% of patients with MS.
Irritability more commonly seen than low self-esteem.
Neurobiology38 – Superior frontal or parietal regions , right temporal lobe
, left medial inferior prefrontal cortical lesions and dominant anterior
temporal atrophy
Factors that worsen the prognosis of illness:
• Suicidal tendency
• Functional disability
• Negative cognitions
Treatment
• Not needed in around 60% patients.
• Low dose antidepressants ( Sertraline/ Desipramine) with CBT -
preferred CHRI, 2018 49
50. PSYCHOSIS & MS
33,39
Though rare (2-3%) , seen generally in the later stages of MS
Symptoms seen – somatic delusions; disorganized behavior; rarely
hallucinations (visual & auditory)
Affective psychosis more common when compared to schizophrenia.
Increased activation of inflammatory signaling pathways and altered anti-
inflammatory activity are common factors in the pathophysiology of MS and
psychotic disorders.
Seen in patients with periventricular involvement (temporal region)
Treatment – low dose atypical antipsychotics in combination with MS
treatment (steroids and IFN) with proper supervision
CHRI, 2018 50
52. • Mr. A, a 27-year-old single male , pure vegetarian presented to OPD with
following symptoms of 1 year duration.
• Forgetfulness for several weeks, followed by social withdrawal, paucity of speech,
decreased interest in routine and pleasurable activities and apathy ; stopped
going to his work and taking household responsibilities unlike his previous self.
His self-care deteriorated markedly, appetite decreased grossly and he lost 5–7 kg
weight in 4–5 months. His duration of sleep also increased.
• Patient was started on Tab. Olanzapine 5 mg/d considering the option of negative
symptoms of schizophrenia .
• Over the next 3–4 weeks, he perceived minimal improvement, but developed b/l
weakness of lower limbs resulting in limping and walking with support. He was
referred to neurology opd.
• On detailed examination and investigations, he was diagnosed with sub acute
CASE VIGNETTE – 445
CHRI, 2018 52
53. VITAMIN B12
DEFICIENCY
Water-soluble essential vitamin, has a
vital role in DNA synthesis during cell
division.
Linked with synthesis of neurotransmitters
46,47
Psychiatric manifestations 48,49 of vitamin
B12 deficiency include
• Depression
• Apathy
• Irritability
• Dementia
• Catatonia
• Delirium
• Hallucinations CHRI, 2018 53
54. VITAMIN B12
DEFICIENCY47
POOR INTAKE
Chronic alcohol use
Vegetarian diet
MALABSORPTION:
Lack of Intrinsic Factor
Ileal malabsorption
Bacterial overgrowth
DEFECTIVE
TRANSPORT
(GENETIC):
Transcobalamin
deficiency.
CHRI, 2018 54
55. Around 28% patients with B12 deficiency manifest initially
with psychiatric manifestations
Prevalence of neuropsychiatric manifestations in patients
with Vit-B12 deficiency ranges from 10-20% , more common
in elderly.
Comorbid Psychiatric condition or psychiatric manifestation
due to Vitamin B12 deficiency – Both tend to improve
symptomatically with parenteral cobalamin.
CHRI, 2018 55
56. NEUROPSYCHIATRIC MANIFESTATIONS
OF VIT-B12 DEFICIENCY 48,49
Biochemical Basis – Defect in methylation process 50
DEPRESSION
(38%)
Predominant depressive cognitions,
anhedonia , easy fatigability and somatic
symptoms
PSYCHOSIS
(1-16%)
Prominent Schneiderian first rank
symptoms
(Thought alienation; 3rd person AH;
Somatic passivity; Delusion of persecution
& reference)
BPAD Classical Manic features
CHRI, 2018 56
57. ALZHIEMERS
Severe naming
problems Paraphasias
Ideomotor Apraxia
COMMONLY
IMPAIRED IN BOTH
GROUPS
Concentration
Abstraction
Visuo-spatial
orientation
Categorization
VIT-B12 DEFICIENCY
DEMENTIA
Frequent Psychotic
symptoms
Mild naming problems
CHRI, 2018 57
58. CENTRAL
PONTINE
MYELINOLYSIS
Common clinical
manifestations
• Spastic quadriparesis
• Dysarthria
• Pseudo bulbar palsy
• Altered mental status.
Severe cases - locked-in
syndrome or even death can
occur.
Lesion – Symmetrical Butterfly
shaped area of demyelination
within the central pons. 52
DEFINITION: Clinically heterogeneous,
demyelinating condition originally
thought to occur only in the central
pons 51
Risk factors: 52
• Hyponatremia for > 24 hours
• Over-correction of hyponatremia (> 25
mEq/L/day)
• Rapid correction (greater than 1–2 meq/hr)
• Alcoholism
• Malnutrition
• Liver disease CHRI, 2018 58
60. Demyelination of ascending fibers of RAS in
pons
Disruption of RAS pathway to thalamic nuclei
Affects several NT pathways
Acute change in behavior
CHRI, 2018 60
61. PSYCHIATRIC MANIFESTATIONS
• Psychiatric manifestations with CPM are rare.
• If present, seen after 2 weeks of onset of motor symptoms
• Few symptoms seen with CPM53 are
Emotional liability(crying)
Formal thought disorder
Delirium
Confusion
Personality change
Hallucinations
Delusions of persecution and reference
CHRI, 2018 61
62. METACHROMATIC
LEUKODYSTROPHY54
•MLD in adolescence or early adulthood presents as psychosis in 53
% individuals (Disorganized cognitive processes, delusions and
auditory hallucinations).
•Normally in Psychosis, gray matter ( limbic areas & temporal lobe)
affected; While in MLD, there is demyelination of frontal white
matter
•The neuropathalogical correlation in MLD suggests that psychosis
can result from dysfunctional connectivity between certain extra
frontal and subcortical structures with the frontal lobe.
•Other psychiatric complaints are very rare.
CHRI, 2018 62
63. TREATMENT FOR
NEUROPSYCHIATRIC
MANIFESTATIONS IN
DEMYELINATING DISORDERS
DEPRESSION
•CANMAT GUIDELINES prefer use of
anti-depressants in comorbid mood
disorders.55
•SSRI or SNRI – preferred drug
•TCA (Desipramine)
•MAOI (Moclobemide)
•ECT (can worsen neurocognition).
•Antidepressants with CBT
•To be monitored for SWITCH in the
BIPOLAR DISORDER56
Based on side-effect profile
•Lithium
•Anticonvulsants
•Atypical antipsychotics
High risk patients –
prophylactically addition of mood
stabilizer to be considered.
CHRI, 2018 63
64. ANXIETY57
•SSRI & SNRI –preferred
•Benzodiazepines –
used for short-term
PSYCHOSIS 58
More prone to develop EPS
Atypical antipsychotics – better risk
vs. benefit
Ziprasidone, risperidone, and
aripiprazole - First-line
CHRI, 2018 64
66. STEROIDS 59, 60
•Used for almost all autoimmune and
most of demyelinating disorders
•Psychiatric manifestations :
Mild & reversible after
withdrawal or decreasing steroid
dose.
Old age – High risk
•Affective disorders - Family history of
depression & Substance use
•Psychotic Disorder – SLE;
Hypoalbuminemia; Higher dose of
steroids;
•10% cases – Psychotropic medications
needed
Commonly seen are :
• Emotional liability
• Sleep Disturbances
• Hypomania
• Mania
• Depression
• Psychosis
• Delirium(older patients)
• Cognitive changes and
memory deficits
CHRI, 2018 66
67. Widely used in the treatment of
milder forms of SLE, RA and
Sjogrens syndrome
In SLE - added to steroid therapy
In RA - used along with NSAIDs
and DMARDs.
Neuropsychiatric symptoms:
mild and transient.
Headache and dizziness.
Emotional disturbances,
agitation, insomnia,
nightmares, anxiety, fatigue.
Psychotic symptoms are
relatively rare.
INTERFERON 63
Used as treatment for MS and
other demyelinating disorders.
Most commonly seen
psychiatric illness – Depression
(5-25%)
Others :
• Anxiety (1.5-4%)
• Mania(less than 1%)
• Psychosis (less than 1%)
CHRI, 2018 67
68. TAKE HOME POINTS
•Missing an autoimmune or demyelinating disorder as a psychiatric disorder
can, sometimes, have serious and fatal consequences.
•Prodromal cases or milder cases may continue to be treated as psychiatric
disorders and hence a high index of suspicion is required to diagnose these
disorders , particularly in those with positive family history of autoimmune
disorders.
•Basic knowledge of these conditions is necessary to think of them, in case of
atypical presentation or refractory cases.
•Most of them being chronic illnesses, mood and anxiety disorders are more
prevalent and psycho education and CBT helps in them.
•In case of psychotic conditions, Typical antipsychotics should preferably be
avoided in these conditions.
CHRI, 2018 68
69. TO SUSPECT AUTOIMMUNE /
DEMYELINATING DISORDER WHEN
•Fatigue or cognitive impairment out of proportion to the
mood symptoms or depression
•Atypical presentation
•Not responding to anti-depressants or anti-psychotics
•Presence of EPS with minimal dose of typical anti-
psychotics
•To monitor BP and electrolytes if we suspect any
autoimmune disorders
CHRI, 2018 69
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Few-(SLE)- diag criteria
Others- sx are due to chronic disease
, prevent binding of BDNF , and
GENES : inherited ; only around 10% to 15% of the inherited risk for ADs can be explained at present
Immune cells damage tissues directly by killing cells or indirectly by releasing cytotoxic cytokines, prostaglandins, ROS .
Tissue macrophages and monocytes can act as antigen presenting cells to initiate an autoimmune response, or as effector cells once an immune response has been initiated.
Macrophages act as killer cells through antibody-dependent cell-mediated cytotoxicity and by secreting Th1 cytokines, which act as protein signals between cells. Macrophages and neutrophils damage tissues by releasing cytotoxic proteins, e.g., nitric oxide and hydrogen peroxide. Cytokines and other mediators released by macrophages recruit other inflammatory cells such as neutrophils and T cells, to the site of inflammation
Autoantibodies appear long before clinical symptoms thus providing a good predictive marker for the potential to develop disease. In fact, the risk of developing an AD goes from about 10% if one autoantibody is present to around 60–80% and if three autoantibodies are present for a particular AD
Within two days, patient showed marked improvement. Her catatonic symptoms totally disappeared, she became communicative, her affect improved. Retrospective delusions of reference and persecution were found. Risperidone was gradually tapered off. On two follow-ups, after two and four weeks of steroid therapy, the patient was symptom-free.
Less sleep and appetite/wt loss ; poor concentration
Connective tissue – cartilage / lining of blood vessels
fatigue, malaise and low-grade intermittent fever; migratory arthritis or arthralgia develops in majority of cases.
other skin changes like purpura, alopecia or photosensitivity
Auto-antibodies enter the brain causing neuronal damage, including impaired neuroplasticity and synaptic transition.
To reach the brain, BBB must be transiently breached by external (for example, infection) or internal (for example, metabolic derangement, cytokines) triggers. Vascular injury can be antibody mediated by aPL antibodies or via accelerated classical atherosclerosis.
RISK FACTORS
Anxiety- young age
Psychosis- presenting manifestation of SLE in 60% pts
Components more common to least
Cognitive dysfunction is common and may include apraxia, aphasia, and agnosia along with impairments in abstract thinking, short- and long-term memory, judgment, and visual–spatial function
Pred- 20mg or more
Neural - myelitis
pro-inflammatory cytokines are IL-1B, IL-6, and TNFα ---- activate HPA axis
cytokine serum levels seem to be positively correlated with sx -- appetite loss, anorexia, weight loss, fatigue, sleep disturbances, motor retardation, reduced libido, cognitive impairment, anhedonia, and depressed mood, which are frequent in depressive disorders.12
Inspite of treatment induced mood sx, steroids preferred drug of choice.
onset of altered mental status, rigidity, hyperthermia, and autonomic instability
Prodromal phase (Phase 1) – headaches or a viral-like fever (headaches, respiratory, and gastrointestinal symptoms) seen in more than 80% of patients.
.Illness Phase (Phase 2)
Psychiatric phase – 2 wks after initial phase.
Progressive decline in speech and language which may include alogia, echolalia, perseveration
Paediatric population often manifests with manic symptoms, irritability, behavioural outbursts, sleep dysfunction, hyperactivity and hypersexuality
Neurological Complications:
.Recovery and relapse phase (Phase 3) :
Some patients have a prolonged course of illness but can show spontaneous neurological improvement.
Cognitive and psychiatric functions are the slowest to improve. Relapse rate of 20% to 25%.
. Late Phase (Phase 4):
85% of patients with full recovery of significant cognitive behavioural abnormalities on the hospital discharge, may have deficits in executive function, impulsivity, behavioural disturbance and abnormal sleep pattern
all patients have intrathecal synthesis of antibodies recognizing the NMDA receptor
MRI- normal in 50%
EEG is usually abnormal, showing slow and disorganized activity in the delta/theta range
Normally, excitatory glutamate stimulates NMDAR receptors in the interneuron resulting in GABA release and GABA, in turn, inhibits the release of dopamine from the mesolimbic pathway. Thus the glutamatergic pathway acts as a break on the mesolimbic dopamine pathway.
If NMDA receptors are hypoactive, then the tonic inhibition on the mesolimbic dopamine pathway will not occur, resulting in hyperdopaminergia and an increase in the dopamine in the mesolimbic system resulting in positive symptoms.
NNAI – non neurological autoimmune
Infectious : agents might cause psychosis directly (by affecting the neurons and the brain) or indirectly (by activating the immune system).
Autoimmune mech:
2 hit model : Perinatal activation of microglia leads to a primed state. stress in adolescence triggers pathological overactivation, leading to cortical loss and the development of symptoms.
Inflammation : the complement system (a component of the immune response) is more active in both autoimmune disorders and schizophrenia
Genes :
Social stigma – self conscious / helpless/embarrassed
Poor coping -- avoiding being in public, indulging in over-eating and alcohol abuse
When unadressed ----- Depresion & anxiety
Stress --- activates sympathetic nervous system --- increase NA and adrenaline---- reduce cortisol--- dysregulates HPA axis- cutaneous system– upregulates pro-inflammatory cytokines (IL-1, IL-6, TNF-α) ---- Increases the itch
Depression – more of sleep /sexual / anxiety sx / fatigue / poor interaction
Sexual – Depression ; Substance dependence or abuse etc.
Sleep - initial insomnia, an increase of nocturnal awakenings, early morning awakenings, and daytime sleepiness.
presents with fatigue, weakness, abdominal pain, nausea, vomiting, weight loss, and skin hyperpigmentation
Crisis- Medical emergency; delirium and other sx..
Hypothyroid + Addisons – SCHMIDT syndrome.
Abn EEG even after addisons resolution – persistent brain damage & subtle cognitive changes
GC R more in hippocampus ----- low- hippocampal synaptic circuit impaired. GC r – PFC – (recent study)
Anter pitutry – secretes precursor- proopiomelanocortin (pomc)
AH /Visual halluci – rarely
DEPRESSION- emotional withdrawal / apathy/ loss of initiation
Co-morbid psychiatric symptoms that appear during the course of the illness may be misdiagnosed as true myasthenic symptoms leading to unnecessary drug treatment
Coinciding psych sx--- such as fatigue, lack of energy and shortness of breath
Sleep dist -- Central cholinergic deficit, such a consequence of nocturnal respiratory problems, nonspecific immunological processes or as a result of increased mental fatigue
relationship between emotional status and the initial presentation of MG, as well as flare-up
Corticosteroids, one of the available therapies for MG, are associated with psychiatric manifestations.
antiphospholipid antibodies are detected in up to 50% of patients with SLE
Primary APS- venous and arterial thrombosis (mainly in cerebral vascular bed), habitual abortions and other pregnancy complications with the coexistence of antiphospholipid antibodies, including lupus anticoagulant, anticardiolipin antibodies, and/or antibodies to beta2 glycoprotein I
Cognitive impairment- can be discrete / sever – amnesia.
Other autoimmune- less common w.r.t SLE / APS
Sjogrens- sicca syndrome / Anti-rho antibodies detected
Systemic sclerosis - fibrosis of the skin, subcutaneous tissue, and internal organs (lungs, kidneys, heart ant gastrointestinal tract) causing their failure
impaired morphology of blood vessels leading to Raynaud’s phenomenon and primary arterial pulmonary hypertension, and immune system abnormalities
affect mainly peripheral nervous system
Long-acting benzodiazepines are associated with excessive night time sedation or respiratory depression
Myasthenia -- agents with anticholinergic effect such as olanzapine, quetiapine and clozapine avoided
Psoriasis – fluoxetine seem to worsen skin condition
Valproic acid and topiramate were not found to affect MG
Lithium carbonate - cause new-onset myasthenic symptoms and exacerbation of MG – propranolol used
Carbamazepine interferes with the bioavailability of immunosuppressants
Demyelination – progressive axonal loss
Biperiden – anti-Parkinson drug ; weak peripheral anti-cholinergic.
Pt improved in 40 days
Pathogenesis of multiple sclerosis and critical roles of GPCRs. Studies with genetic manipulations and/or pharmacological interventions suggest that GPCRs mediate important processes in the development of EAE or MS: (I) T-cell activation; (II) T-cell egress from lymphoid tissues; (III) migration and infiltration of inflammatory cells from the periphery to the CNS; (IV) BBB integrity maintenance; (V) astrocyte activation; (VI) microglia activation; (VII) demyelination and neurotoxicity.
Jean Martin Charcot – first gave diag criteria
Visual & somato sensory evoked potentials
Fatigue – physical & mental
------------Poor QOL
MACFIMS - five cognitive domains commonly impaired in MS such as IPS/working memory, learning and memory, executive function, visual-spatial processing, and language
Only antipsychotics – don’t show much improvement
inflammatory signaling pathways (such as NF-κB pathways)
Euphoria - mood of cheerful complacency out of context with the patient’s total situation.
differed from the elation of hypomania in not being accompanied by motor restlessness, increased energy or speeding up of thought process
PBA- disconnection syndrome resulting in the loss of brainstem inhibition of a putative center for laughing and crying
ALCOHOL – worsen cognitive sx
CANNABIS – relieve pain & spasticity
During this entire period, patient or family members denied history of any pervasive sad mood or any othe mood or psychotic symptoms.
NT – DA ;5HT – pathogenesis of various neuropsych disorders
Lack of intrinsic factor – Pernicious anemia / atrophic gastritis/ post gastrectomy
Ileal malabs : Ileal resection / crohns disease
4-6% of psychiatric inpatients had vit-B12 deficiency
CD – no ideomotor apraxia / language ipairment
acute and often fatal complication of alcoholism
25% patients – extra pontine areas also involved
These symptoms can be delayed, occurring 2 to 14 days after rapid correction of hyponatremia
Vomiting, confusion, disordered eye movements and coma are common.
locked in’ syndrome with mutism and paralysis but relatively intact sensation and comprehension
Predilictn for PONS- grid arrangement of oligodendrocytes in pons – limits mechanical flexibility – swells
over-rapid correction of low serum sodium
the pons being unusually vulnerable to rapid changes in electrolyte balance due to its close admixture of white matter bundles and richly vascular grey matter
Extra pontine – often b/l- m/c sites -cerebellar peduncles, globus pallidus, thalamus, LGB & putamen.
Reticular activating system
Ar inheritance / deficiency of Arylsulfatase A
Early adult (12-30yrs)
Assess adherence at every consultation / psychoeducation.
SSRI/SNRI – better tolerated
TCA – more anti-cholinergic – poor tolerated
Anti-dep + cbt : interest to meet the particular needs of each individual patient whenever possible
Li- poor tolerated because of diuresis
Antipsych – more prone to EPS ( in demyelinating dis)
Anti-convulsants - sedation, dizziness, headaches, ataxia, tremors, nausea, constipation, and weight gain
More risk for tardive dyskinesia compared to other EPS sx.
Side-effects more with higher dose.( more than 20gm prednisone)
Psychotropics- 2 weeks to act
Sleep prob- may interfere with normal pattern of diurnal cortisol synthesis
Initially- agitation/euphoria/hypomania/mania
Longstanding- Depression
antibodies bind the NMDA receptor, leading to its internalization from the cell surface and a state of relative NMDA receptor hypofunction.
this removes the tonic inhibition on dopamine released in the mesolimbic pathway resulting in psychosis
diagnosis is suspected if the patient presents psychiatric symptoms (e.g., early age of onset, catatonia), neurological signs, resistant or intolerance to antipsychotic treatment, history of autoimmune disorder, and severe infections. The diagnosis relies on the detection in the circulation of autoantibodies and, particularly, directed against neurotransmitter receptors, such as the glutamate NMDA receptor.