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INTRODUCTION
ο‚— Many medical conditions have neurologic and psychiatric symptoms
ο‚— early identification of the underlying cause can be critical in directing
further management
ο‚— Medical conditions known to cause neuropsychiatric symptoms are
extensive, can also be varied in presentation, making diagnosis
challenging
Medical conditions with neuropsychiatric manifestations
System Disease
Infectious HIV/AIDS
Opportunistic infections/malignancies
Syphilis
Lyme disease
Prion disease
Rheumatologic/autoimmune Systemic lupus erythematosus
Sarcoidosis
Vasculitides
Multiple sclerosis
Endocrinologic Hypothyroidism/hyperthyroidism
Hypoparathyroidism/hyperparathyroidi
sm
Cushing syndrome
Adrenal insufficiency
Neoplastic Paraneoplastic syndromes
CNS tumors (primary and metastatic)
Carcinomatous meningitis
Medical conditions with neuropsychiatric manifestations
System Disease
Metabolic Vitamin deficiencies
Thiamine (vitamin B1)
Vitamin B12
Micronutrient abnormalities
Hypocalcemia/hypercalcemia
Acute hepatic porphyrias
Wilson disease
Amyloidosis
Hepatic encephalopathy
Uremia
Hematologic Sickle cell disease (cerebrovascular
disease)
Heritable/genetic Huntington disease
Lysosomal storage diseases
INFECTIOUS
COVID-19
ο‚— Various adverse neurological and psychiatric outcomes occurring after
COVID-19 have been predicted and reported
ο‚— COVID-19 was associated with increased risk of neurological and
psychiatric outcomes
ο‚— the risk of cerebrovascular events (ischaemic stroke and intracranial
haemorrhage) was elevated after COVID-19
ο‚— significantly increased risk of psychotic disorders
Human Immunodeficiency Virus
ο‚— can cause neuropsychiatric manifestations as a result of primary HIV disease
ο‚— associated or comorbid with HIV disease include
οƒ˜ minor cognitive impairment
οƒ˜ Dementia
οƒ˜ Delirium
οƒ˜ Polyneuropathy
οƒ˜ bipolar affective disorder
οƒ˜ major depression
οƒ˜ Schizophrenia
οƒ˜ Substance abuse
Syphilis
ο‚— Neurosyphilis was once common, occurring in up to 40% of patients with
documented syphilis
ο‚— Neuropsychiatric symptoms caused by syphilis are usually late manifestations of
the disease
ο‚— Early neurosyphilis can be either asymptomatic (diagnosed based on CSF studies)
or symptomatic presenting with
οƒ˜ acute meningitis
οƒ˜ leptomeningeal spread
οƒ˜ CNS inflammation (gummas)
οƒ˜ ophthalmologic symptoms (uveitis)
οƒ˜ otic symptoms (hearing loss)
οƒ˜ meningovascular symptoms
ο‚— Treatment of neurosyphilis requires parenteral antibiotics intravenous (IV)
penicillin G for 10 to 15 days or procaine penicillin G intramuscularly and oral
probenecid for 10 to 14 days
ο‚— Ceftriaxone and doxycycline may be reasonable alternatives in patients who are
allergic to penicillin
Lyme Disease
ο‚— caused by Borrelia burgdorferi, can present with neurologic manifestations
ο‚— Spirochetes seed the nervous system and can cause a variety of neurologic
symptoms
ο‚— Many patients with erythema migrans can have fatigue,headache, and
cognitive impairment
ο‚— Approximately 15% of patients develop meningitis, cranial neuropathies, or
radiculopathy/radiculitis acutely early neuroborreliosis
ο‚— Peripheral
ο‚— neuropathies (including radiculopathy, symmetric polyneuropathies, and
carpal tunnel syndrome) and encephalomyelitis can occur
ο‚— Electromyogram/nerve conduction studies can be helpful to characterize
peripheral nervous systems disorders
RHEUMATOLOGIC
ο‚— Several autoimmune/rheumatologic diseases can cause neuropsychiatric symptoms
ο‚— systemic lupus erythematosus (SLE), sarcoidosis, CNS vasculitis, and multiple sclerosis are
common.
ο‚— Most patients with SLE develop neuropsychiatric symptoms
Data from The American College of Rheumatology nomenclature and case definitions for neuropsychiatric lupus
syndromes. Arthritis Rheum 1999;42(4):599–608.
Sarcoidosis
ο‚— can present with a large variety of both systemic and neuropsychiatric
symptoms
ο‚— It is estimated that 5% to 15% of patients with sarcoidosis develop
related neurologic symptoms
ο‚— Sarcoidosis can affect both the central and peripheral nervous systems,
and most frequently causes cranial neuropathies
ο‚— Neurosarcoidosis can cause nearly any neurologic symptom, including
οƒ˜ aseptic meningitis
οƒ˜ Seizures
οƒ˜ peripheral neuropathies
οƒ˜ psychiatric symptoms
οƒ˜ small fiber neuropathies
ENDOCRINOLOGIC
Thyroid Disorders
ο‚— Both hypothyroidism and hyperthyroidism can cause neuropsychiatric symptoms
ο‚— Hypothyroidism can cause cognitive impairment and symptoms of depression.
ο‚— autoimmune thyroiditis (Hashimoto disease) is associated with encephalopathy
ο‚— Hypothyroidism is also associated with
οƒ˜ Ataxia
οƒ˜ peripheral neuropathies (including carpal tunnel syndrome and symmetric
polyneuropathies
οƒ˜ Myopathies
ο‚— Hyperthyroidism can also cause both CNS and peripheral nervous system
syndromes
οƒ˜ Psychiatric symptoms such as irritability and anxiety
οƒ˜ in the elderly, depression and lethargy
οƒ˜ Patients can present with cognitive deficits (memory impairment, inattention, and
decreased productivity)
οƒ˜ tremor and seizures
οƒ˜ peripheral neuropathies
οƒ˜ myasthenia gravis
οƒ˜ hypokalemic periodic paralysis
οƒ˜ myopathy
Cushing Syndrome
ο‚— Hypercortisolism (Cushing syndrome) causes neuropsychiatric symptoms in
more than 50% of patients.
ο‚— Common psychiatric symptoms include
οƒ˜ Dysphoria
οƒ˜ irritability, appetite changes
οƒ˜ anxiety and panic attacks
οƒ˜ mania, psychosis, and insomnia
ο‚— Excess cortisol can also have profound effects on cognitive function
ο‚— Cushing syndrome are commonly left with residual psychiatric symptoms and
cognitive impairment
Addison Disease
ο‚— deficiencies in glucocorticoids, aldosterone, and
androgens, can also cause nonspecific systemic symptoms
that overlap with psychiatric symptoms
ο‚— chronic adrenal insufficiency can have neuropsychiatric
symptoms including
οƒ˜ cognitive impairment
οƒ˜ Depression
οƒ˜ psychosis
METABOLIC
Vitamin Deficiencies
ο‚— Vitamin deficiencies can also cause neuropsychiatric symptoms
ο‚— Thiamine deficiency classically causes Wernicke-Korsakoff syndrome(Wernicke
encephalopathy (WE) and Korsakoff syndrome)
ο‚— Cobalamin deficiency can cause a wide range of neuropsychiatric symptoms
Data from Stabler S, Allen R. Cecil textbook of medicine. Philadelphia: Saunders; 2004. p. 1054–5
Calcium Disorders
ο‚— Both hypocalcemia and hypercalcemia can cause neuropsychiatric
manifestations
ο‚— Hypocalcemia can cause seizures and increased neuromuscular
excitability, as well as psychiatric symptoms such as emotional lability,
depression, psychosis, and anxiety
ο‚— Hypercalcemia can cause confusion, lethargy, generalized weakness,
and in severe cases coma and death
Porphyrias
ο‚— Acute porphyrias can cause neurologic and psychiatric symptoms
ο‚— These acute porphyrias typically present with neurovisceral symptoms: the classic
triad consists of abdominal pain, peripheral neuropathy, and altered mental
status.
ο‚— isolated reports of neuropathy, encephalopathy, or psychosis
ο‚— Psychiatric symptoms are present in more than half of patients with symptomatic
acute porphyria
ο‚— psychiatric sequelae commonly include psychotic disorders, but can also include
depression, anxiety, and delirium
ο‚— Patients often require hospitalization for acute attacks
Wilson Disease
ο‚— Wilson disease is a rare, autosomal recessive disorder of copper
transport
ο‚— Neurologic sequelae can include choreoathetosis,dysarthria, dystonia,
tremor, ataxia, parkinsonism, and cognitive impairment
ο‚— early diagnosis and treatment can prevent severe neurologic
ο‚— symptoms and appropriately treated patients can even have a normal
life span
NEOPLASTIC
Paraneoplastic Syndromes
Paraneoplastic syndromes may affect the peripheral nervous system or CNS.
NEUROPSYCHIATRIC MANIFESTATIONS IN
NEUROLOGICAL DISORDERS
NEUROANATOMICAL PERSPECTIVES
π—ˆ Cerebral white matters are reciprocally connected to parietal,
Temporal and occipital lobes in addition to extensive subcortical
connection.
π—ˆ Ratio of white to grey matter is significantly higher in the right
than the left hemisphere particular is in frontal lobes.
π—ˆ Groups of white matter pathways are recognised which completely
myelinate in II or III decade.
They are projection, Commissural and Association fibres.
π—ˆ Salient physiological aspect is the presence of myelin which results in
marked increase in axonal conduction velocity.
π—ˆ The potential recovery is grater in white matter disorders than is grey
matter disorders.
π—ˆ Finally white matter figures prominently in a general theory of
brain-behaviour relationships due to its multiple networks of
interconnected neurons that subservice various behavioural
functions.
C E R E B R A L WHITE M AT T E R D I S O R D E R A N D B E H AV I O U R
Disorder Pathology Clinical features
Clinical
pathological
correlation
Multiple sclerosis Inflammatory
demyelination
Cognitive loss
Demention Mood
disorders
Strong
Toluene
leukoencohalopat
hy
Toxic
demyelination
Cognitive loss
Apathy Dementia Strong
Binswanger’s
disease
Ischemic
Demyelination
Apathy
Abulia
Dementia
Strong
Traumatic brain
injury
White matter
shearing
Attention
Dement ion
Depression
Strong
Disorder
Pathology
Clinical features
Clinical
pathological
correlation
Metachromatic
leukodystrophy
Dysmyelination Mental Retardation
Psychosis Demention Strong
Cobalamin
deficiency
White matter
degeneration
Cognitive loss
Demention
Psychosis
Strong
AIDS
demention
complex
White matter
pallor
Cognitive loss Apathy
Dementia Moderate
Normal pressure
hydrocephalus
white matter
compression
Cognitive loss Apathy
Dementia Moderate
Pathology
NEUROBEHAVIORAL FUNCTIONS
π—ˆ Attention
π—ˆ Memory
π—ˆ Language
π—ˆ Visio spatial ability
π—ˆ Complex
π—ˆ Emotional Competence
BEHAVIOUR O C C U R R I N G IN ALZHEIMER’S
D I S E A S E A N D T H E R E P O R T E D I N F L U E N C E O F I N C R E A S E D O R D E C R E A S E D
C H O L I N E R G I C A C T I V I T Y E A C H B E H A V I O U R .
Behaviour Reduced cholinergic function Enhanced cholinergic
function
Psychosis Delusion is common in AD
Thought disorder in AD
Is increased with anticholinergic
medications delusions correlat
with cholinergic deficiency in low
body demention
Delusions occur in anti
cholinergic delirium
Anti cholinergic agents
exacerbate Schizophrenia
Nicotinic receptors are reduced in
Schizophrenia
Delusions in ad are decreased
by physostigmine
Delusion in delirium are
Decreased by physostigmine
Physostigmine may reduced
Psychosis in schizophrenia
Nicotinic therapy normalizes
Electro physiologic
abnormalities in
schizophrenia
Behaviour Reduced cholinergic
function
Enhanced cholinergic
function
Depression Major depression is rare in AD
Anticholinergic drugs reduce
depression in some depressed
individuals
Anticholinergic agents produce
euphoria there is long REM latency
in AD
REM latency is prolonged by
anticholinegric agents Abnormal
DST in AD
Abnormal DS with
Anticholinergics
Cholinergic agents produce
depression in some a patients
Cholinergic hypersensitivity
produce a depression
syndrome in animals
Anticholinergic agents have
anti manic effects REM
latency is shortened in
depression
REM latency is shortened by
Cholinergic agents
Cholinergic agents increase
serum cortisol
Behaviour Reduced cholinergic function Enhanced cholinergic
function
Agitation Increased in AD increased in AD
treated with anticholinergic agents
Reduced by physostigme in AD
Personality Apathy is common in ad reduced
affinitive behaviour induced by
Anticholinergic agents
Apathy in AD is reduced by
Tacrine
NEURO PSYCHIATRIC SYMPTOMS
π—ˆ Apathy
π—ˆ Agitation
π—ˆ Anxiety
π—ˆ Irritability
π—ˆ Dysphoria
π—ˆ Aberrant motor behaviour
π—ˆ Disinhibition
π—ˆ Delusion
π—ˆ Hallucination
π—ˆ Euphoria
π—ˆ Night time behaviour disturbance
π—ˆ Appetite and eating abnormality
N E U R O L O G I C A L C O N D I T I O N S P R E S E N T I N G WITH
P S YC H I AT R I C A N D B E H AV I O U R P R O B L E M S .
π—ˆ Summarises the primary C N S disorders
associated with the 5 major psychiatric
symptoms.
π—ˆ Depression
π—ˆ Anxiety
π—ˆ Psychosis
π—ˆ Mania
π—ˆ Aggression
Primary C N S
Disorders
Dep Anx Psy Man Agg
Dementia/retardation + + + +
Alzheimer disease + + + +
Huntington’s chores + + + +
Other dementias + + + + +
Mental retardation + + + + +
Epilepsy (especially +
temporal lose)
+ + + +
ganglia
E xtraphyamidal
disorder
C alcinations of basal +
Dep Anx Psy Man Agg
Parkinson’s disease + + + +
Progressive supranulear palsy +
Wilson’s disease + + +
Frontal lobe syndrome
infection
Aids + + +
Neurosyphilis + + +
Encephalitis meningitis + + +
Migraine +
Multiple sclerosis + + + + +
Dep Anx Psy Man Agg
Pseudo bulbar palsy +
Strokes + + + + +
Traumatic brain injury + + + +
Tumours
CNS Tumours + +
Temporal lobe
tumours
+ + + +
Medication Dep Anx Psy Man Agg
Anticholinergic + +
Antidepressants +
Antihistamines +
Antihypertensive + + +
Baclofen +
Barbiturates + + +
Cimetidine +
Corticosteroids + + + + +
Decongestants + +
Dep Anx Psy Man Agg
Estrogen + +
Insulin +
Interferon + +
Isoniazed +
Levodopa and other
dopamine agonists
+ + + +
Neuroepletics + +
Nonsterodial anti-inflam + + +
Opioids +
MEDICAL Dep Anx Psy Man Agg
Sympathomimetics/brinchodila
ntors
+ +
Thyroid preparation +
Drugs of abuse
Alcohol intoxication + + + + +
Alcohol withdrawal + + + +
Amphetamine intoxication + +
Amphetamine withdrawal + + +
Benzodiazepine intoxication +
Benzodiazepine withdrawal + + +
ME DICA L Dep Anx Psy Man Agg
Caffeine withdrawal + + +
Cociane intoxication + + +
Marijuana intoxication + +
Opiate intoxication + +
Phencyclidine intoxication + + + +
T H E E VA LUAT I O N O F PSYCHIATRIC SYTEMS:
π—ˆ Medical history
π—ˆ For hyper metabolic syndromes
π—ˆ For aggression
π—ˆ Psychiatric history
π—ˆ For depression
π—ˆ For hyper metabolic syndromes
π—ˆ Medication
π—ˆ Physical examination
π—ˆ Mental status
π—ˆ For suicide attempt
π—ˆ Laboratory investigation
π—ˆ For anxiety
π—ˆ For hyper metabolic syndromes
CLINICALLY INDICATED:
π—ˆ Chest x ray
π—ˆ Electrocardiogram
π—ˆ E E G
π—ˆ Head CT/MRI
π—ˆ Lumber puncture
π—ˆ RPR
π—ˆ HIV
π—ˆ FOR depression:
π—ˆ Cortisol levels
π—ˆ For anxiety:
π—ˆ Plasma catecholamine
PSYCHOSIS:
π—ˆ Head trauma
π—ˆ SOL
π—ˆ Vascular insults
π—ˆ CNS infection
π—ˆ Huntington
π—ˆ Alzheimers
π—ˆ Picks
CLINICAL CLUES:
π—ˆ If sudden, it is likely to be acute encephalopathy
π—ˆ If the symptoms are chronic, hallucinations and
delusions are added and tend to be associated with
dementia or static Encephalopathy
π—ˆ Psychosis with delusional belief are common in
subcortical disorders associated with extrapyramidal
symptoms,
TREATMENT
π—ˆ 4 POINT leather restriants
π—ˆ Haloperidol or droperidol
π—ˆ Lorazepam if agitation is more
π—ˆ D 1 Receptor blocking neuroleptics may be used.
π—ˆ If Medical workup does not indicate an etiology,
psychiatric hospitalization
MANIA
Mania is a mood disturbance accompanied by
π—ˆ Decreased sleep
π—ˆ Racing thoughts
π—ˆ Increased talkativeness
π—ˆ Distractibility
π—ˆ Increased activity
The neurological conditions associated with it are
π—ˆ Temporal lobe seizure
π—ˆ Ms
π—ˆ Right hemispheric strokes
π—ˆ Central nervous spine tumors
TREATMENT
π—ˆ Mild symptoms -Lithium carbonate
-Valproate
-Benzodiazepine
π—ˆ Severe symptoms - Neuroleptic
- ECT
HYPERMETABOLIC SYNDROMES
π—ˆ muscle rigidity
π—ˆ Hyperthermia
π—ˆ Autonomic Dysfunction
They are
N M S
Serotonin Syndrome
Malignant hyperthermia
Lethal Catatonias
MANGEMENT
π—ˆ Medical causes to be excluded
π—ˆ Supportive cate- Temp. Control, Hydration
π—ˆ Treatment of complication
-Hypertension
- Cardiac Arrhythmias
- Divc
- Rhabdomyolysis with renal failure
-Pulmonary Embolism
AMNESTIC SYNDROMES
π—ˆ Impairment of short term and long term memory occurring in a
normal of consciousness.
π—ˆ The pattern of memory loss follows RIBOT’S LAW
CLINICAL C LU E S
Syndrome/ Etiology
Characteristics
- Acute (Wernicke’s
encephalopathy)
- Chronic (Korsakoff
amenesia)
Oculomotor signs, ataxia
Wernince- Korsakoff syndrome delirium
Severely impaired
anterograde memory
Associated with
confabulation
Syndrome/ Etiology Characteristics
Trasient global amnesia Anteto grade amnesia during
episode
Duration of a few hours
History of trauma
Brief period of retrograde amnesia
Variable period antero gade
amnesia
Head trauma History of trauma
Brief period of retrograde amnesia
Variable period antero grade
amnesia
Alcohol related blackout Aassociated with prolonged
alcohol abuse and severe
intoxication
Syndrome/ Etiology
ο‚— Loss of memory for time
following a traumatic event
itself
ο‚— Loss of primary
autobiographical material
Normal short memory
ο‚— May not be concerned about
symptoms
Characteristics
Epilepsy May be associated with
motor abnormalities
Benzodizepine or other
Medication usage
Consciousness often
disturbed impairment short
term memory
Dissociative amesia
Syndrome/ Etiology Characteristics
Dissociative fugue Sudden unexpected travel away from
home inability to recent pasts
Loss of personal identity
Amenesi a associated
with stroke
Often PCA distribution infarcts (bilateral)
Hypoxic episode
Often accompanied by focal deficits such
as hemianpsia, cortical blindness visual
agonsia.
Dementia Memory impairment in the setting of
other cognitive deficits that impair daily
living.
Electroconvulsive therapy Only after repeated sessions
Deficits resolve within 6 months
TREATMENT
π—ˆ Memory impaired - complete and behavior
rehabitation
π—ˆ Wernicke’s Encephalopathy - Thiamine
π—ˆ TGA- No independent risk factor for stroke
- 94%
- 5-7%
TGA
Can develop epilepsy
π—ˆ Dissociate amnesia – psychiatrist management
CO NC LUSIONS
π—ˆ Psychiatric consultation may clarify the presence of a
primary psychiatric condition
π—ˆ β€œThe great majority of us are required to live a life of
constant systematic duplicity. Your health is bound to be
affected if day after day you say the opposite of what you
feel; if you grovel before what you dislike and rejoice at
what bring you nothing but misfortune. The nervous
system is not just a fiction it is part of our physical body
and our soul exists in space and inside us; like the teeth
in our mouth. It can’t forever be treated with impunity,”
Medical conditions with NeuroPsychiatric problems

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Medical conditions with NeuroPsychiatric problems

  • 1.
  • 2. INTRODUCTION ο‚— Many medical conditions have neurologic and psychiatric symptoms ο‚— early identification of the underlying cause can be critical in directing further management ο‚— Medical conditions known to cause neuropsychiatric symptoms are extensive, can also be varied in presentation, making diagnosis challenging
  • 3. Medical conditions with neuropsychiatric manifestations System Disease Infectious HIV/AIDS Opportunistic infections/malignancies Syphilis Lyme disease Prion disease Rheumatologic/autoimmune Systemic lupus erythematosus Sarcoidosis Vasculitides Multiple sclerosis Endocrinologic Hypothyroidism/hyperthyroidism Hypoparathyroidism/hyperparathyroidi sm Cushing syndrome Adrenal insufficiency Neoplastic Paraneoplastic syndromes CNS tumors (primary and metastatic) Carcinomatous meningitis
  • 4. Medical conditions with neuropsychiatric manifestations System Disease Metabolic Vitamin deficiencies Thiamine (vitamin B1) Vitamin B12 Micronutrient abnormalities Hypocalcemia/hypercalcemia Acute hepatic porphyrias Wilson disease Amyloidosis Hepatic encephalopathy Uremia Hematologic Sickle cell disease (cerebrovascular disease) Heritable/genetic Huntington disease Lysosomal storage diseases
  • 6. COVID-19 ο‚— Various adverse neurological and psychiatric outcomes occurring after COVID-19 have been predicted and reported ο‚— COVID-19 was associated with increased risk of neurological and psychiatric outcomes ο‚— the risk of cerebrovascular events (ischaemic stroke and intracranial haemorrhage) was elevated after COVID-19 ο‚— significantly increased risk of psychotic disorders
  • 7. Human Immunodeficiency Virus ο‚— can cause neuropsychiatric manifestations as a result of primary HIV disease ο‚— associated or comorbid with HIV disease include οƒ˜ minor cognitive impairment οƒ˜ Dementia οƒ˜ Delirium οƒ˜ Polyneuropathy οƒ˜ bipolar affective disorder οƒ˜ major depression οƒ˜ Schizophrenia οƒ˜ Substance abuse
  • 8. Syphilis ο‚— Neurosyphilis was once common, occurring in up to 40% of patients with documented syphilis ο‚— Neuropsychiatric symptoms caused by syphilis are usually late manifestations of the disease ο‚— Early neurosyphilis can be either asymptomatic (diagnosed based on CSF studies) or symptomatic presenting with οƒ˜ acute meningitis οƒ˜ leptomeningeal spread οƒ˜ CNS inflammation (gummas) οƒ˜ ophthalmologic symptoms (uveitis) οƒ˜ otic symptoms (hearing loss) οƒ˜ meningovascular symptoms ο‚— Treatment of neurosyphilis requires parenteral antibiotics intravenous (IV) penicillin G for 10 to 15 days or procaine penicillin G intramuscularly and oral probenecid for 10 to 14 days ο‚— Ceftriaxone and doxycycline may be reasonable alternatives in patients who are allergic to penicillin
  • 9. Lyme Disease ο‚— caused by Borrelia burgdorferi, can present with neurologic manifestations ο‚— Spirochetes seed the nervous system and can cause a variety of neurologic symptoms ο‚— Many patients with erythema migrans can have fatigue,headache, and cognitive impairment ο‚— Approximately 15% of patients develop meningitis, cranial neuropathies, or radiculopathy/radiculitis acutely early neuroborreliosis ο‚— Peripheral ο‚— neuropathies (including radiculopathy, symmetric polyneuropathies, and carpal tunnel syndrome) and encephalomyelitis can occur ο‚— Electromyogram/nerve conduction studies can be helpful to characterize peripheral nervous systems disorders
  • 10. RHEUMATOLOGIC ο‚— Several autoimmune/rheumatologic diseases can cause neuropsychiatric symptoms ο‚— systemic lupus erythematosus (SLE), sarcoidosis, CNS vasculitis, and multiple sclerosis are common. ο‚— Most patients with SLE develop neuropsychiatric symptoms Data from The American College of Rheumatology nomenclature and case definitions for neuropsychiatric lupus syndromes. Arthritis Rheum 1999;42(4):599–608.
  • 11. Sarcoidosis ο‚— can present with a large variety of both systemic and neuropsychiatric symptoms ο‚— It is estimated that 5% to 15% of patients with sarcoidosis develop related neurologic symptoms ο‚— Sarcoidosis can affect both the central and peripheral nervous systems, and most frequently causes cranial neuropathies ο‚— Neurosarcoidosis can cause nearly any neurologic symptom, including οƒ˜ aseptic meningitis οƒ˜ Seizures οƒ˜ peripheral neuropathies οƒ˜ psychiatric symptoms οƒ˜ small fiber neuropathies
  • 13. Thyroid Disorders ο‚— Both hypothyroidism and hyperthyroidism can cause neuropsychiatric symptoms ο‚— Hypothyroidism can cause cognitive impairment and symptoms of depression. ο‚— autoimmune thyroiditis (Hashimoto disease) is associated with encephalopathy ο‚— Hypothyroidism is also associated with οƒ˜ Ataxia οƒ˜ peripheral neuropathies (including carpal tunnel syndrome and symmetric polyneuropathies οƒ˜ Myopathies ο‚— Hyperthyroidism can also cause both CNS and peripheral nervous system syndromes οƒ˜ Psychiatric symptoms such as irritability and anxiety οƒ˜ in the elderly, depression and lethargy οƒ˜ Patients can present with cognitive deficits (memory impairment, inattention, and decreased productivity) οƒ˜ tremor and seizures οƒ˜ peripheral neuropathies οƒ˜ myasthenia gravis οƒ˜ hypokalemic periodic paralysis οƒ˜ myopathy
  • 14. Cushing Syndrome ο‚— Hypercortisolism (Cushing syndrome) causes neuropsychiatric symptoms in more than 50% of patients. ο‚— Common psychiatric symptoms include οƒ˜ Dysphoria οƒ˜ irritability, appetite changes οƒ˜ anxiety and panic attacks οƒ˜ mania, psychosis, and insomnia ο‚— Excess cortisol can also have profound effects on cognitive function ο‚— Cushing syndrome are commonly left with residual psychiatric symptoms and cognitive impairment
  • 15. Addison Disease ο‚— deficiencies in glucocorticoids, aldosterone, and androgens, can also cause nonspecific systemic symptoms that overlap with psychiatric symptoms ο‚— chronic adrenal insufficiency can have neuropsychiatric symptoms including οƒ˜ cognitive impairment οƒ˜ Depression οƒ˜ psychosis
  • 17. Vitamin Deficiencies ο‚— Vitamin deficiencies can also cause neuropsychiatric symptoms ο‚— Thiamine deficiency classically causes Wernicke-Korsakoff syndrome(Wernicke encephalopathy (WE) and Korsakoff syndrome) ο‚— Cobalamin deficiency can cause a wide range of neuropsychiatric symptoms Data from Stabler S, Allen R. Cecil textbook of medicine. Philadelphia: Saunders; 2004. p. 1054–5
  • 18. Calcium Disorders ο‚— Both hypocalcemia and hypercalcemia can cause neuropsychiatric manifestations ο‚— Hypocalcemia can cause seizures and increased neuromuscular excitability, as well as psychiatric symptoms such as emotional lability, depression, psychosis, and anxiety ο‚— Hypercalcemia can cause confusion, lethargy, generalized weakness, and in severe cases coma and death
  • 19. Porphyrias ο‚— Acute porphyrias can cause neurologic and psychiatric symptoms ο‚— These acute porphyrias typically present with neurovisceral symptoms: the classic triad consists of abdominal pain, peripheral neuropathy, and altered mental status. ο‚— isolated reports of neuropathy, encephalopathy, or psychosis ο‚— Psychiatric symptoms are present in more than half of patients with symptomatic acute porphyria ο‚— psychiatric sequelae commonly include psychotic disorders, but can also include depression, anxiety, and delirium ο‚— Patients often require hospitalization for acute attacks
  • 20. Wilson Disease ο‚— Wilson disease is a rare, autosomal recessive disorder of copper transport ο‚— Neurologic sequelae can include choreoathetosis,dysarthria, dystonia, tremor, ataxia, parkinsonism, and cognitive impairment ο‚— early diagnosis and treatment can prevent severe neurologic ο‚— symptoms and appropriately treated patients can even have a normal life span
  • 22. Paraneoplastic Syndromes Paraneoplastic syndromes may affect the peripheral nervous system or CNS.
  • 24. NEUROANATOMICAL PERSPECTIVES π—ˆ Cerebral white matters are reciprocally connected to parietal, Temporal and occipital lobes in addition to extensive subcortical connection. π—ˆ Ratio of white to grey matter is significantly higher in the right than the left hemisphere particular is in frontal lobes. π—ˆ Groups of white matter pathways are recognised which completely myelinate in II or III decade. They are projection, Commissural and Association fibres.
  • 25. π—ˆ Salient physiological aspect is the presence of myelin which results in marked increase in axonal conduction velocity. π—ˆ The potential recovery is grater in white matter disorders than is grey matter disorders. π—ˆ Finally white matter figures prominently in a general theory of brain-behaviour relationships due to its multiple networks of interconnected neurons that subservice various behavioural functions.
  • 26. C E R E B R A L WHITE M AT T E R D I S O R D E R A N D B E H AV I O U R Disorder Pathology Clinical features Clinical pathological correlation Multiple sclerosis Inflammatory demyelination Cognitive loss Demention Mood disorders Strong Toluene leukoencohalopat hy Toxic demyelination Cognitive loss Apathy Dementia Strong Binswanger’s disease Ischemic Demyelination Apathy Abulia Dementia Strong Traumatic brain injury White matter shearing Attention Dement ion Depression Strong
  • 27. Disorder Pathology Clinical features Clinical pathological correlation Metachromatic leukodystrophy Dysmyelination Mental Retardation Psychosis Demention Strong Cobalamin deficiency White matter degeneration Cognitive loss Demention Psychosis Strong AIDS demention complex White matter pallor Cognitive loss Apathy Dementia Moderate Normal pressure hydrocephalus white matter compression Cognitive loss Apathy Dementia Moderate Pathology
  • 28. NEUROBEHAVIORAL FUNCTIONS π—ˆ Attention π—ˆ Memory π—ˆ Language π—ˆ Visio spatial ability π—ˆ Complex π—ˆ Emotional Competence
  • 29. BEHAVIOUR O C C U R R I N G IN ALZHEIMER’S D I S E A S E A N D T H E R E P O R T E D I N F L U E N C E O F I N C R E A S E D O R D E C R E A S E D C H O L I N E R G I C A C T I V I T Y E A C H B E H A V I O U R . Behaviour Reduced cholinergic function Enhanced cholinergic function Psychosis Delusion is common in AD Thought disorder in AD Is increased with anticholinergic medications delusions correlat with cholinergic deficiency in low body demention Delusions occur in anti cholinergic delirium Anti cholinergic agents exacerbate Schizophrenia Nicotinic receptors are reduced in Schizophrenia Delusions in ad are decreased by physostigmine Delusion in delirium are Decreased by physostigmine Physostigmine may reduced Psychosis in schizophrenia Nicotinic therapy normalizes Electro physiologic abnormalities in schizophrenia
  • 30. Behaviour Reduced cholinergic function Enhanced cholinergic function Depression Major depression is rare in AD Anticholinergic drugs reduce depression in some depressed individuals Anticholinergic agents produce euphoria there is long REM latency in AD REM latency is prolonged by anticholinegric agents Abnormal DST in AD Abnormal DS with Anticholinergics Cholinergic agents produce depression in some a patients Cholinergic hypersensitivity produce a depression syndrome in animals Anticholinergic agents have anti manic effects REM latency is shortened in depression REM latency is shortened by Cholinergic agents Cholinergic agents increase serum cortisol
  • 31. Behaviour Reduced cholinergic function Enhanced cholinergic function Agitation Increased in AD increased in AD treated with anticholinergic agents Reduced by physostigme in AD Personality Apathy is common in ad reduced affinitive behaviour induced by Anticholinergic agents Apathy in AD is reduced by Tacrine
  • 32. NEURO PSYCHIATRIC SYMPTOMS π—ˆ Apathy π—ˆ Agitation π—ˆ Anxiety π—ˆ Irritability π—ˆ Dysphoria π—ˆ Aberrant motor behaviour π—ˆ Disinhibition π—ˆ Delusion π—ˆ Hallucination π—ˆ Euphoria π—ˆ Night time behaviour disturbance π—ˆ Appetite and eating abnormality
  • 33. N E U R O L O G I C A L C O N D I T I O N S P R E S E N T I N G WITH P S YC H I AT R I C A N D B E H AV I O U R P R O B L E M S . π—ˆ Summarises the primary C N S disorders associated with the 5 major psychiatric symptoms. π—ˆ Depression π—ˆ Anxiety π—ˆ Psychosis π—ˆ Mania π—ˆ Aggression
  • 34. Primary C N S Disorders Dep Anx Psy Man Agg Dementia/retardation + + + + Alzheimer disease + + + + Huntington’s chores + + + + Other dementias + + + + + Mental retardation + + + + + Epilepsy (especially + temporal lose) + + + + ganglia E xtraphyamidal disorder C alcinations of basal +
  • 35. Dep Anx Psy Man Agg Parkinson’s disease + + + + Progressive supranulear palsy + Wilson’s disease + + + Frontal lobe syndrome infection Aids + + + Neurosyphilis + + + Encephalitis meningitis + + + Migraine + Multiple sclerosis + + + + +
  • 36. Dep Anx Psy Man Agg Pseudo bulbar palsy + Strokes + + + + + Traumatic brain injury + + + + Tumours CNS Tumours + + Temporal lobe tumours + + + +
  • 37. Medication Dep Anx Psy Man Agg Anticholinergic + + Antidepressants + Antihistamines + Antihypertensive + + + Baclofen + Barbiturates + + + Cimetidine + Corticosteroids + + + + + Decongestants + +
  • 38. Dep Anx Psy Man Agg Estrogen + + Insulin + Interferon + + Isoniazed + Levodopa and other dopamine agonists + + + + Neuroepletics + + Nonsterodial anti-inflam + + + Opioids +
  • 39. MEDICAL Dep Anx Psy Man Agg Sympathomimetics/brinchodila ntors + + Thyroid preparation + Drugs of abuse Alcohol intoxication + + + + + Alcohol withdrawal + + + + Amphetamine intoxication + + Amphetamine withdrawal + + + Benzodiazepine intoxication + Benzodiazepine withdrawal + + +
  • 40. ME DICA L Dep Anx Psy Man Agg Caffeine withdrawal + + + Cociane intoxication + + + Marijuana intoxication + + Opiate intoxication + + Phencyclidine intoxication + + + +
  • 41. T H E E VA LUAT I O N O F PSYCHIATRIC SYTEMS: π—ˆ Medical history π—ˆ For hyper metabolic syndromes π—ˆ For aggression π—ˆ Psychiatric history π—ˆ For depression π—ˆ For hyper metabolic syndromes π—ˆ Medication π—ˆ Physical examination π—ˆ Mental status π—ˆ For suicide attempt π—ˆ Laboratory investigation π—ˆ For anxiety π—ˆ For hyper metabolic syndromes
  • 42. CLINICALLY INDICATED: π—ˆ Chest x ray π—ˆ Electrocardiogram π—ˆ E E G π—ˆ Head CT/MRI π—ˆ Lumber puncture π—ˆ RPR π—ˆ HIV π—ˆ FOR depression: π—ˆ Cortisol levels π—ˆ For anxiety: π—ˆ Plasma catecholamine
  • 43. PSYCHOSIS: π—ˆ Head trauma π—ˆ SOL π—ˆ Vascular insults π—ˆ CNS infection π—ˆ Huntington π—ˆ Alzheimers π—ˆ Picks
  • 44. CLINICAL CLUES: π—ˆ If sudden, it is likely to be acute encephalopathy π—ˆ If the symptoms are chronic, hallucinations and delusions are added and tend to be associated with dementia or static Encephalopathy π—ˆ Psychosis with delusional belief are common in subcortical disorders associated with extrapyramidal symptoms,
  • 45. TREATMENT π—ˆ 4 POINT leather restriants π—ˆ Haloperidol or droperidol π—ˆ Lorazepam if agitation is more π—ˆ D 1 Receptor blocking neuroleptics may be used. π—ˆ If Medical workup does not indicate an etiology, psychiatric hospitalization
  • 46. MANIA Mania is a mood disturbance accompanied by π—ˆ Decreased sleep π—ˆ Racing thoughts π—ˆ Increased talkativeness π—ˆ Distractibility π—ˆ Increased activity The neurological conditions associated with it are π—ˆ Temporal lobe seizure π—ˆ Ms π—ˆ Right hemispheric strokes π—ˆ Central nervous spine tumors
  • 47. TREATMENT π—ˆ Mild symptoms -Lithium carbonate -Valproate -Benzodiazepine π—ˆ Severe symptoms - Neuroleptic - ECT
  • 48. HYPERMETABOLIC SYNDROMES π—ˆ muscle rigidity π—ˆ Hyperthermia π—ˆ Autonomic Dysfunction They are N M S Serotonin Syndrome Malignant hyperthermia Lethal Catatonias
  • 49. MANGEMENT π—ˆ Medical causes to be excluded π—ˆ Supportive cate- Temp. Control, Hydration π—ˆ Treatment of complication -Hypertension - Cardiac Arrhythmias - Divc - Rhabdomyolysis with renal failure -Pulmonary Embolism
  • 50. AMNESTIC SYNDROMES π—ˆ Impairment of short term and long term memory occurring in a normal of consciousness. π—ˆ The pattern of memory loss follows RIBOT’S LAW CLINICAL C LU E S Syndrome/ Etiology Characteristics - Acute (Wernicke’s encephalopathy) - Chronic (Korsakoff amenesia) Oculomotor signs, ataxia Wernince- Korsakoff syndrome delirium Severely impaired anterograde memory Associated with confabulation
  • 51. Syndrome/ Etiology Characteristics Trasient global amnesia Anteto grade amnesia during episode Duration of a few hours History of trauma Brief period of retrograde amnesia Variable period antero gade amnesia Head trauma History of trauma Brief period of retrograde amnesia Variable period antero grade amnesia Alcohol related blackout Aassociated with prolonged alcohol abuse and severe intoxication
  • 52. Syndrome/ Etiology ο‚— Loss of memory for time following a traumatic event itself ο‚— Loss of primary autobiographical material Normal short memory ο‚— May not be concerned about symptoms Characteristics Epilepsy May be associated with motor abnormalities Benzodizepine or other Medication usage Consciousness often disturbed impairment short term memory Dissociative amesia
  • 53. Syndrome/ Etiology Characteristics Dissociative fugue Sudden unexpected travel away from home inability to recent pasts Loss of personal identity Amenesi a associated with stroke Often PCA distribution infarcts (bilateral) Hypoxic episode Often accompanied by focal deficits such as hemianpsia, cortical blindness visual agonsia. Dementia Memory impairment in the setting of other cognitive deficits that impair daily living. Electroconvulsive therapy Only after repeated sessions Deficits resolve within 6 months
  • 54. TREATMENT π—ˆ Memory impaired - complete and behavior rehabitation π—ˆ Wernicke’s Encephalopathy - Thiamine π—ˆ TGA- No independent risk factor for stroke - 94% - 5-7% TGA Can develop epilepsy π—ˆ Dissociate amnesia – psychiatrist management
  • 55. CO NC LUSIONS π—ˆ Psychiatric consultation may clarify the presence of a primary psychiatric condition π—ˆ β€œThe great majority of us are required to live a life of constant systematic duplicity. Your health is bound to be affected if day after day you say the opposite of what you feel; if you grovel before what you dislike and rejoice at what bring you nothing but misfortune. The nervous system is not just a fiction it is part of our physical body and our soul exists in space and inside us; like the teeth in our mouth. It can’t forever be treated with impunity,”