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.
5. HISTORY
In early 1900s, for the first time , an association between neuropsychiatric symptoms and
infectious organisms was made in patient with syphilis (Hideyo et.al), followed by patients
affected in viral influenza epidemic.
Later many theories were put forth and research was done to find the etiology of
neuropsychiatric complaints in patients with infectious diseases.
Few of the accepted mechanisms are – direct effect on CNS , autoimmune process, altered
neurotransmitter function, or influence of infectious organisms at a critical developmental
period .
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6. INTRODUCTION
Infectious organisms can play an important role in pathophysiology of
neurodegenerative and neurobehavioral diseases 1
Psychiatric symptoms can be associated with several systemic and central nervous
system infections and they can be the initial presenting symptoms, occurring in the
absence of neurological symptoms in some disorders2
Maternal and childhood infections are considered as risk factors for psychosis 3
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8. Possible Mechanism of Psychiatric
manifestations in Infectious diseases
Depressive
Symptoms 5
• As a process of immune response, IFN-gamma is responsible to activate
indoleamine-2, 3-dioxygenase and deplete tryptophan , which results in
decreasing serotonin production.
Delirium 6
• High levels of pro-inflammatory cytokines and cortisol in CSF
• Presence of elevated C-reactive protein
Psychotic
symptoms 7
• Following certain infections , there is up-regulation of MicroRNA-132 , which is
associated with changes in dopamine receptor signaling
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9. NEUROSYPHILIS
Neurosyphilis (NS) occurs in up to 30% of people with untreated syphilis and may occur at
any stage of the infection
It has a wide spectrum of neurocognitive symptoms that, apart from being non-specific, are
also common to many neurologic and psychiatric disorders which makes the diagnosis
difficult.
The frequency of psychiatric symptoms associated with NS reported in literature ranges
from 33% - 86%. 7
The most common presenting neuropsychological symptoms being personality change and
hallucinations (in 48% of patients).
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10. CLASSIFICATION OF NEUROSYPHILIS 8
• Syphilitic meningitis - result of direct meningeal
inflammation, rarely has focal findings.
• Meningovascular syphilis - ischemic changes caused
by proliferative endarteritis, causing permanent CNS
damage, and presents most commonly as a stroke
syndrome.
• Parenchymatous neurosyphilis (general paresis or
tabes dorsalis), there is direct neural destruction
resulting in diminished neuron concentration,
demyelination, and gliosis.
• Gummatous neurosyphilis, the mass effect causes
neurologic manifestations
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11. AS per ICD-10
F02.8 : Dementia in other specified diseases classified elsewhere
Dementia can occur as a manifestation or consequence of a variety of cerebral and
somatic conditions.
Includes – Dementia in Neurosyphilis (A52.1)
A50.4 Late congenital neurosyphilis [juvenile neurosyphilis]
A52.1 Symptomatic neurosyphilis
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12. GENERAL PARESIS
(DEMENTIA PARALYTICA)
Because of the cognitive loss and neuropsychiatric disturbances associated with tertiary neurosyphilis.
Generally starts 10 to 20 years after infection, seen in 5-15% of patients.
Spirochetes can be demonstrated in the tissues of the brain, and the pathology is thought to be due to
the irritation produced by these spirochetes in the brain parenchyma.
Neuroimaging studies 9
• Frontocortical atrophy and disseminated high signal lesions in a frontal distribution;
• SPECT imaging reveals a marked reduction in cerebral perfusion, particularly in the bilateral
frontal and temporal cortices.
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13. CLINICAL FEATURES
Prodromal symptoms (Headache , insomnia , lethargy )
Insidious change in the personality ( apathy , emotional lability , irritability)
Delirium
Episodic forgetfulness – first cognitive change
Other cognitive changes:
Difficulty with calculation
disturbances of speech and writing
Impaired insight
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14. SIMPLE DEMENTING FORM 10
Impairment of memory
Early loss of insight
Delirium
Associated with mild euphoria or apathy or fleeting, ill-systematized persecutory
delusions.
The patients are mostly quiet, lethargic and amenable throughout the course of
the disease.
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15. GENERAL PARESIS PRESENTING AS OTHER
FORMS 10
• More of elated mood , grandiose delusions.
• If his beliefs are questioned, the mood readily turn to irritability
or anger.
EXPRESSIVE
OR
GRANDIOSE
FORM
• Low mood, Suicidal thoughts, Delusions (Nihilism ,
hypochondriacal or guilt)
• Symptoms are out of proportionate to signs
DEPRESSIVE
FORM (27%)
• Delusion of persecution – more common
• Associated with schizophrenic symptoms like – somatic passivity
,commanding hallucinations.
PSYCHOTIC
FEATURES
(Very rare)
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16. NEUROLOGICAL FEATURES ON
EXAMINATION 11
Abnormal pupils
Tremors
Dysarthria
Deep tendon reflex abnormalities
Cerebellar signs ( incoordination ,Gait ataxia, Positive Romberg’s sign )
Other conditions may be associated :
Seizures
Hemiparesis
Autistic features
Parkinsonism features
Huntington's chorea
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17. MANAGEMENT
Goal - to reverse the manifestations or arrest the disease progression.
Any psychiatric medication – to be started in low dose and monitored for side-effects
Anti-psychotics - Quetiapine and Aripiprazole preferred.
ECT – AVOIDED (worsens neurological signs & impaired overall prognosis)
Rehabilitation (if deficits persist)
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18. MENINGITIS
Meningitis commonly presents with Pyrexia & neck stiffness , hence diagnosis is not missed.
In general , 95% of individuals present with at least two of the four cardinal symptoms:
headache, fever, neck stiffness and altered mental status.
However, in some conditions, the presenting complaints may be vague and presents with altered
sensorium or personality changes.
Broadly 3 types of meningitis are discussed – Bacterial , Aseptic and Tubercular meningitis.
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19. MENINGITIS
Inflammation of Meninges
Disrupted blood supply to nerve cells(affected by toxins)
Damage to nerve cells
Fluid leak into brain tissue
Brain swelling
Raised ICT
Interrupt oxygen supply to brain tissue
That part of the brain is injured or damaged
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20. MENINGITIS EARLY
SYMPTOMS
PSYCHIATRIC
SYMPTOMS
Other features Neurological
abnormality
BACTERIAL 12
(Neisseria meningitidis,
Streptococcus pneumoniae,
Staphylococcus aureus, Haemophilus
infl uenzae and E. coli)
Headache ,
vomiting,
photophobia,
irritability
Delirium,
Fatigue, Depression,
Personality change,
mood lability
Cerebellar
symptoms;
Sluggish DTRs;
Seizures
Damage in
Cortical and
subcortical areas
ASEPTIC 12
Most common - Viral
(Enterovirus; HSV;VZV;EBV)
(Rarely - early stages of TB
meningitis, brain abscess,
neurosyphilis, leptospirosis)
Malaise
Fever
Muscle and joint
aches
Tiredness, Irritability,
Reduced
concentration, Mood
swings and
Depression
Recurring
headaches.
TUBERCULAR 13
Prodromal phase
(headache ,
Anorexia)
Apathy, Psychosis,
irritability and
insidious change of
personality.
Coarse Tremors,
Abnormal
reflexes,
3,6,7 cranial
nerve palsies,
Hemiplegia,
Seizures,
Papilledema
Subependymal
Tubercles;
Rupture of bacilli
into sub-
arachnoid
hemorrhage.
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21. NEURO-PSYCHIATRIC SYMPTOMS
AS SEQUALAE OF MENINGITIS 14
BACTERIAL • Insomnia
• Cognitive impairment
• Depression
ASEPTIC • Depression
• Insomnia
• Anxiety
• Neuro-cognitive impairment
TUBERCULAR Retrograde Amnesia and
amnesia for active illness
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22. COGNITIVE IMPAIRMENT 15
Generally seen in patients with both bacterial and viral , more common with bacterial
(Pneumococcal and meningococcal meningitis - around 30%)
Domains involved are:
• Impairment of memory
• Decreased psychomotor performance
• Impaired attention/executive functions
• Reduction in visuoconstructive capacity
Male sex and cranial nerve involvement were predictors of poor cognitive outcomes.
In Children :
• Persistent learning difficulties
• Deficits in Short-term memory
• Poor Academic performance
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23. TUBERCULOSIS
Chronic infectious multi systemic disease caused by mycobacterium tuberculosis and is one of the
leading causes of mortality worldwide
A higher rate of mortality and morbidity was seen among patients with baseline psychiatric illness ,
because they defaulted from treatment
There is a high prevalence of psychiatric illness in TB patients, but primary care physicians and
specialists do not screen this association although anxiety and depression occur frequently in
persons with these cases.16
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24. NEUROPSYCHIATRIC MANIFESTATIONS 17
Prevalence in patients with TB – 31%
• Depression (19-26%)- Most common
• Anxiety
• Substance Use Disorder
• Personality changes
Co-infection with HIV may significantly increase the risk of depression by up to 70%
Associated with
• increase in the number of symptoms reported
• more serious perceived consequences
• less control over the illness
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25. Psychological reaction to the diagnosis or
treatment (TB)
1. Social stigma
• External: rejection, blame &
discrimination
• Internal: shame, guilt, social
withdrawal, isolation, depression
2. Social/occupational/functional impairment
3. Infectiousness/household exposure
Vulnerable populations
Poverty
Seriously mentally ill
Homeless
Co infected with HIV
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27. MALARIA
Malaria can sometimes be presented with unusual
features
1. due to the development of immunity
2. the increasing resistance to anti-malarial drugs
3. the indiscriminate use of antimalarial drugs.
Cerebral malaria is the most dreaded and a potentially
life-threatening complication.
Cerebellar ataxia, extrapyramidal rigidity and various
psychiatric symptoms have been described either as the
early manifestations of cerebral malaria or as a part of
the post malaria neurological syndrome
19
.
• Endothelial
damage
Induction of
NO
• Alteration of Vascular
Permeability
Inhibits NMDA channel
in post-synaptic cell.
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28. NEUROPSYCHIATRIC MANIFESTATIONS 20
RISK FACTORS
• High grade fever
• Alcohol
• Financial or inter
personal stressors
• Exacerbation of pre-
existing psychiatric illness
Symptoms/Disorders
• Acute psychosis
• Mania
• Delirium
• Catatonic symptoms
• Mood disorders (rare)
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29. MALARIAL PSYCHOSIS 20
Develops because of encephalopathy in patients with cerebral malaria.
Manifests as paranoid and manic syndromes in the acute stage, depression being a late
sequelae.
Agitation and confusion may develop after the patient has recovered from coma.
Sometimes, these psychiatric manifestations may be the presenting features in patients with
acute uncomplicated malaria, especially in association with hyperpyrexia
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30. Post-Malaria Neurological Syndrome (PMNS) 21
Seen after symptomatic malarial infection & clearance of parasites from blood.
It is characterized by development of neurological and psychiatric symptoms that can occur 1
- 4 months after exposure.
Clinical manifestations:
o GTCS
o Delayed cerebellar ataxia
o Psychosis
o Tremors
Generally seen in patients with severe malaria and those treated with mefloquine treatment
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31. Neuropsychiatric impairments due to cerebral malaria in children :
Long-term cognitive impairment
Acquired language disorder
Inattention
Impulsiveness and hyperactivity
Conduct disorders
Impaired social development
Obsessive symptoms
Self-injurious behaviors
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32. PSYCHIATRIC MANIFESTATIONS
DUE TO ANTI MALARIAL DRUGS
MEFLOQUINE
22
• Anxiety
• Paranoia
• Depression and
suicidality
• Hallucinations, and
psychotic Behaviour
CHLOROQUINE
23
• Increased psycho-
motor activity
• Disorientation
• Incoherent speech
• Confusion
• Outbursts of abnormal
behavior
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33. NEUROCYSTICERCOSIS
Common neuroparasitic infection with a worldwide distribution.
Endemic in rural areas of the developing countries of Asia, Africa, Latin America, and central
Europe.
Characterized by the deposition of cysticerci in the brain as a result of eating of undercooked
pork.
Responsible for nearly half of the late onset cases of epilepsy in the endemic areas and is also
associated with psychiatric manifestations 24
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34. Parietal lobe was the most affected area, followed by frontal lobe and disseminated lesions. 25
Left sided lesions were associated with more psychiatric morbidity.
Neuro-psychiatric Manifestations:
Focal seizures (68%)
Depression (52%)
Psychotic disorders(14%)
Cognitive impairment(80%)
Catatonic or manic symptoms
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35. HSV ENCEPHALITIS
Causative organism HSV -2 virus
Population Neonatal and immunocompromised
Clinical presentation Acute fever , with delirium , behavioral abnormalities like
personality changes, hallucinations, florid psychotic symptoms.
Focal deficits can result in seizures or myoclonus
Kluver-Bucy Syndrome
EEG Periodic temporal spikes and slow waves
MRI Diffuse inflammation (temporo-parietal region) 26
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36. The prominence of psychiatric disturbance is seen characteristically when the pathology is seen in
the temporal lobes and orbitofrontal structures . 27
Thus, focal symptoms such as anosmia, olfactory and gustatory hallucinations, or marked memory
disturbance out of proportion to the impairment of intellect can also be seen.
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37. SUBACUTE SCLEROSING
PANENCEPHALITIS 28
21 cases per million in India.
The majority of cases have a history of measles infection.
More common in children or adolescent age group.
The initial features of the illness include more subtle cognitive impairment deteriorating into
behavioral disturbance and clear-cut dementia.
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38. Neuropsychiatric manifestations
Insidious intellectual impairment
Poor academic performance
Problems in memory and attention
Nocturnal delirium with hallucinations
Marked lethargy
Occasional disinhibition or irritability
Hypersexuality
Neurological signs:
• Myoclonic jerks of the face, fingers and
limbs
• Athetosis or rapid torsion spasms of the
trunk that lead to sudden stumbles and
falls
• B/L extrapyramidal signs.
• Seizures.
• Aphasia, Apraxia, Akinetic mutism.
EEG : Typically there are high-voltage slow-
wave complexes, synchronous in all leads,
and occurring at fixed intervals of 5–10
seconds along with the myoclonic jerk
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39. FUNGAL INFECTIONS 30,31
Cryptococcal meningitis
Triad of headache, fever and vomiting with Altered sensorium(13-73%)
Neuropsychiatric manifestations may be due to meningeal cryptococcosis and raised intracranial
pressure.
Psychosis most commonly seen (Acute / Brief psychotic episode); Occasionally mania or depression
with psychotic symptoms seen.
Candida infection – Schizophrenia, BPAD , Memory disturbances
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40. OTHER INFECTIOUS DISEASES 3
DISEASE TYPICAL SYMPTOMS PSYCHIATRIC
MANIFESTATIONS
BRUCELLOSIS 32
Malaise, headache, weakness,
myalgia and night sweat,
Lymphadenopathy,
hepatosplenomegaly, spinal
tenderness, sacroiliitis.
Behavioral changes,
Psychosis, stupor, Delirium.
Depression is common in
untreated chronic forms of
brucellosis.
LEPTOSPIROSIS Headache, Malaise, Fever,
Anorexia, Myalgia,
Hepatosplenomegaly,
Lymphadenopathy, Skin rash.
Delirium
Mania & Psychosis
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41. OTHER INFECTIOUS DISEASES 3
DISEASE TYPICAL SYMPTOMS PSYCHIATRIC
MANIFESTATIONS
LYMES DISEASE 33
(Lyme Borreliosis)
Erythema migrans
(at the site of tick bite)
Depression, Dementia,
Schizophrenia, BPAD , Hyper
somnolence, panic attacks,
anorexia nervosa and OCD.
TOXOPLASMOSIS 4
Fever, Myalgia and Malaise
Pneumonia, Myocarditis and
Choroidoretinitis
Delirium, Depression , Anxiety,
Psychosis
WHIPPLE’S DISEASE Arthralgia, Diarrhea, Weight loss Depression, Personality
changes, Dementia
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43. CASE VIGNETTE 34
62-year-old man had become withdrawn, apathetic,
with poor sleep over 2 months.
His GP started treatment with citalopram for a
suspected depressive illness.
Gradually patient became increasingly confused and
agitated and reported seeing frightening people and
animals. On several occasions, he left the house to
chase these intruders away and became lost
He also developed involuntary muscle jerks of the
limbs, and his balance deteriorated.
Citalopram was stopped attributing the symptoms to
an adverse drug reaction, but this did not lead to any
improvement.
During a 2-week IP stay in the hospital, extensive
investigations were undertaken, and a diagnosis of
probable sporadic Creutzfeldt-Jakob disease (CJD)
was made.
Visual hallucinosis with associated agitation and
behavioral disturbance continued and the patient
had several falls on the ward as a result of
attempts to move around despite increasing
ataxia and apraxia
Risperidone was initiated at a low dosage, and
within a few days the patient’s agitation and
psychotic symptoms had lessened and patient
got discharged.
Back at home, the patient’s mobility and
cognitive function continued to steadily decline,
and he became increasingly dependent on his
family and caregivers.
Had increased daytime somnolence, became
bedbound and mute.
Was agitated and had dramatic stimulus-
sensitive myoclonus. (improved with Clonazepam
low dose)
Patient expired 8 months after the onset of the
first symptoms of withdrawal and apathy.
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44. INTRODUCTION
Transmissible spongiform encephalopathies (TSEs)
Unique infectious and invariably fatal neurodegenerative disorders of humans and animals
that result from the misfolding of a normal cell protein(PrPc) into an abnormal protein
(PrPSc).
Share a spongiform degeneration of the brain and a variable amyloid plaque formation
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46. CREUTZFELDT-JAKOB DISEASE
35,36,37
A progressive dementia with extensive neurological signs, due to specific neuropathological
changes (subacute spongiform encephalopathy) that are presumed to be caused by a
transmissible agent.
Onset is usually in middle or later life, typically in the fifth decade, but may be at any adult
age.
The course is sub acute, leading to death within 1-2 years.
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47. SPORADIC CJD
Arises from either spontaneous prion gene
(PRNP) somatic mutation or stochastic prion
protein (PrP) structural change.
Affects men and women equally with average age
of onset is 60 years
Psychiatric manifestations
as early presentation seen in 18-39%
At any Stage of illness in 89%
Supportive of Diagnosis:
EEG- synchronized biphasic or triphasic
sharp wave complexes
Presence of 14 - 3 – 3 protein in CSF
Poor prognosis
Mean duration to onset of symptoms to
death is 6 months (3-12 months)
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48. VARIANT CJD
Transmitted through blood transfusion
Presents with a relatively slow clinical
course.
Somatosensory-evoked responses may
demonstrate minor abnormalities,
indicating central involvement of pain
pathways or thalamic origin for the pain.
Psychiatric manifestations seen in almost
all the patients and is considered as one
of the diagnostic criteria for vCJD.
Median duration of survival - 13 months.
IATROGENIC CJD
Accidental transmission of CJD through surgery or
medical procedure
Also be transmitted to humans by using
inadequately sterilized neurosurgical instruments.
In cases of central transmission (use of inadequately
sterilized neurosurgical instruments or implanted
EEG electrodes) patients mainly manifest with
cognitive decline
While in peripheral cases such as transmission of
CJD via injection of contaminated HGH or
gonadotropins, progressive ataxia followed by
dementia predominate the clinical picture.
Majority of these patients develop myoclonic jerks
Psychiatric symptoms are relatively rare.
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50. DEMENTIA
36
Rapidly progressive (usually in weeks)
Rapidly worsening confusion, disorientation.
Problems with memory, thinking, planning and judgment.
Generally associated with hallucinations.
Other behavioral symptoms seen generally in later stages :
• Agitation (episodic) associated with stimulus induced myoclonus
• Wandering behavior
• Repetitive vocalizations
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51. PSYCHOTIC SYMPTOMS (36.9%)
• Visual hallucinations (+/- other visual
complaints)
• Hallucinations in other modalities
• Extra-campine hallucinations (secondary to
delusional content)
• Delusions ( persecution / infidelity)
MOOD SYMPTOMS (41.7%)
social withdrawal
Irritability
Anxiety
low mood
Suicidal ideas
Emotional lability
More in FEMALES
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52. As per ICD-10 (F02.1)
(Dementia in Creutzfeldt-Jakob disease)
Suspected in all cases of dementia that progresses fairly rapidly over months to 1 or 2 years and that is
accompanied or followed by multiple neurological symptoms.
In some cases, such as the so-called amyotrophic form, the neurological signs may precede the onset of
the dementia.
There is usually a progressive spastic paralysis of the limbs, accompanied by extrapyramidal signs with
tremor, rigidity, and choreoathetoid movements.
Other variants may include ataxia, visual failure, or muscle fibrillation and atrophy of the upper motor
neuron type.
The triad consisting of - rapidly progressing, devastating dementia, - pyramidal and extrapyramidal
disease with myoclonus, and - a characteristic (triphasic) electroencephalogram is thought to be
highly suggestive of this disease.
The rapid course and early motor involvement should suggest Creutzfeldt-Jakob disease.
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53. PSYCHIATRIC MANIFESTATIONS NEUROLOGICAL & OTHER
MANIFESTATIONS
FATAL
FAMILIAL
INSOMNIA 37
Dementia may or
may not be seen
Insomnia (severe- visual fatigue & Diplopia)
Personality changes (Apathy)
Disturbances of attention and vigilance and
working memory
Autonomic disturbances including develop.
Major motor abnormalities consist of ataxia,
spontaneous and evoked myoclonus.
Reduced ACTH & Increased se. cortisol
KURU
37
Dementia seen
only in advanced
stages
Seen in later stages
Emotional incontinence with inappropriate
laughter
Apathetic and withdrawn.
Gait ataxia is accompanied by dysmetria ,
dysarthria leading to frequent falls until the
individual can no longer walk independently
or sit without support.
various Other movement disorders such as
clonus, chorea, and athetosis, and convergent
strabismus
No weakness or rigidity
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54. Treatment For prion diseases
38
Symptomatic and palliative treatment
For psychiatric symptoms
Anti – depressants (better tolerated)
Anti – Psychotics ( increased chance of side-effects ; short term )
Benzodiazepines and Sodium Valproate
(Preferred when psychotic symptoms a/w neurological complains; long term in low doses under
supervision)
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55. TAKE HOME POINTS
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 CNSinfection.
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 adultpatientdevelopsdementiarapidlyand
myoclonus.
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maternal exposure during pregnancy to poliovirus, retrovirus, influenza, measles, rubella, varicella zoster, and bacterial agents has been associated with an increased risk of schizophrenia in the offspring
As a immune mech , ifn gamma
reduced expression of two cytoskeletal proteins in the somatosensory cortex and hippocampus
Meningovascular -- Mild encephalitic symptoms, including personality change, emotional lability, insomnia, and decreased memory
(delirium, dementia, mania, psychosis, personality change, and/or depression)
Dementia resembles picks dementia (fronto temporal)
T2 white matter hyperintensities may reverse after antibiotic therapy.
Prodrome – several months
Personality – disinhibited / indecent
common early changes may suggest frontal lobe --- way of coarsening of behaviour and loss of refinement in the personality.
Grandiose – power, wealth , position
Furthermore,) recommends the application of
14 days IV pencilin G 12 to 24 million units daily in divided doses at 4-hour intervals, or alternatively IM weekly injections 2.4 to 4.8 million units of benzathine penicillin or intramuscular (IM) injections of 2.4 million units of procaine penicillin QID
Rothenhäusler (2007 ----- anti-psychotics.
like , Tuberculous meningitis
Van de Beek et al. (2004)
nerve cells do not receive adequate oxygen and nutrients.
DROWSINESS TO COMA ; sometimes a/w hallucinations and excitement– OCD and dissociation- ocassionaly
ASEPTIC --- CSF negative culture
Tubercular- high risk in HIV infected individuals.
INH -- more than 35% of adverse effects associated with INH were psychiatric in nature
Psychosis – delusions commonly seen
After 4 weeks of starting medications
More common with MDR-TB
Occasionally Psychosis can be the first presentation of cerebral malaria
Hallucination and delusion
Mefloquine-induced psychosis --- prodromal phase of moderate symptoms such as dizziness, insomnia, and generalized anxiety f/b frank psychosis with psychomotor agitation and paranoid delusions
Explained by the fact that a lesion of NCC on the dominant side accounted for the morbidity.
CT- affected area is parietal lobe
KBS- possible complication neurobehavioral condition - characterized by visual agnosia, excessive oral tendencies (putting objects into mouth, licking, biting, chewing, touching with lips, and bulimia), hyper metamorphosis, placidity, altered sexual behavior, and changes in dietary habits
Myoclonia --- periodic, occurring at fixed intervals of 5–10 seconds for hours or days at a time
unusual presentation ---- initially misdiagnosed as behavioral disorders and were treated with psychotropic drugs which further extended the course of the disease.
Without appropriate treatment cryptococcal meningitis is invariably fatal with a mortality of 83% in patients without neuropsychiatric manifestation and 76% in patients with neuropsychiatric manifestation.
acute psychosis can be an early presentation of brucellosis
Sequencing of the prion protein gene (PRNP) showed methionine/valine heterozygosity at the codon 129 polymorphism and no pathogenic mutations.
ATROPHY OF
Cerebral cortex--- loss of memory and mental acuity, and sometimes also visual impairment (CJD).
Thalamus --- insomnia (FFI).
Cerebellum incoordination of body movements (kuru, GSS).
14-3-3 : novel protein released with rapid neuronal loss, is present in CSF after strokes or during encephalitis.
Iatrogenic -- corneal transplantation, implantation of contaminated EEG electrode, implantation of dura matter grafts, and following use of contaminated human growth hormone (HGH) preparations derived from human pituitaries
Systemic-- fatigue, disordered sleep, and decreased appetite
behavioral or cognitive decline -- delusions, hallucinations, delirium, depression, apathy, agitation, confusion, disorientation, memory loss
focal signs such as visual loss, cerebellar ataxia, aphasia, and motor deficits
Generalized , non-epileptic with frequency of 1 Hz.
Visual distortions & agnosia
Content – more of animal
Insomnia – first complaint
pyrexia, hyperhidrosis, tachycardia, hypertension, and cardiac arrhythmia
KURU --- transmitted by ritual cannabilism
vague prodrome - malaise