Psychosis and Memory Loss by Dr. Shivan Mahabir

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Psychosis and Memory Loss

A Case Presentation
By
Dr. Shivan A.C. Mahabir
MB. BS. DM (Psych)

SHO Dr. Kale's Team


Demographics
A.L.
62 years old
Male
White Welsh
Married
Unemployed on Benefits
Presenting Complaint
Cut an electrical cord at home with a piece
of glass x 1/7
Wandering away from home x 1/7
Hearing voices x several days
Hx of Presenting Complaint
Patient was assessed at a home visit by Dr.
Mahabir and CPN Gale.
Fluctuating course.
rd

3 home visit in 2 weeks.


Medication had been increased about 12
days prior to this assessment and had
seemed to be having a positive effect but
then pt began deteriorating again.
Patient reported receiving messages
through the air. Hears voices telling him to
do things.
Hx of Presenting Complaint
The patient was actively hallucinating
during the home visit.
No paranoid speech re neighbour.
No recent alcohol or drug use.
No obvious stressor or trigger noted.
Wife overwhelmed. Scared patient could
have electrocuted himself or set the house
on fire.
Hx of Presenting Complaint
At prior home visit done 1/52 prior, the
patient had been much more lucid and
answered questions appropriately. This
followed an increase in his meds.
Prior to that, 2/7 earlier the patient had been
verbally abusive to the wife. Was confused
and doing inappropriate things eg putting
cans of soda into a shoe. He had not been
sleeping and was walking outside semi
clothed. Accusing wife of being unfaithful.
Far Psychiatric History
Known to Mental Health since age 17-18.
FACE entry from 2013 indicates 3 prior
episodes of DSH by overdose.
Benzodiazepine and Amphetamine misuse.
H/o psychosis both with and without drug
use.
In 2007 40000 pounds in debt and
house was in danger of being
repossessed.
2013 used amphetamine and threatened
neighbour (common thread). Section 136.
When things took a turn...
2014 Diagnosed with paranoid schizophrenia as he
was having auditory hallucinations and persecutory
delusions while euthymic.

Also first recorded discussion of Bipolar Affective


Disorder.

EPSE neck stiffness. Quetiapine reduced and


procyclidine introduced.

August 2014 admitted to the inpatient service. 1st


mention of memory problems

September 2014 memory problems + word finding


difficulties

December 2014 CT Head Normal. Amphetamine use


The evolution continues
Feb 2015 Headache x 3/7
April 2015 Memory problems, disoriented to date
and year. No psychosis. Euthymic. Started on
Reboxetine ? Reason. ?R/O pseudodementia.
July 2015 problems with gait and balance.
Dropping things often. Decreased power in hands.
Dysarthria.
Oct 2015 used amphetamines. UDS also Pos for
opiates. ? Drug contamination. Workup for
dexedrine. Prior 11 yr abstinence after
dexamphetamine Tx @ Whitchurch Hospital -
relapsed after mother's death.
Neurology Input
Decreased distance tolerance. Decreased speed.
Writhing movements. Dysarthria. Regurgitation of
food. Frequent falling forward. Erectile dysfunction.
Frequent urinary incontinence. No bowel
incontinence.

O/E: dyarthria. Frontalis overactivity. Abnormal


writhing movements ?dyskinesia. Blank facies.
Stooped gait. Slowed walking and turning. No tremor.
Subtle cogwheeling on distraction.
Dysdiadochokinesia++. Truncal instability ++
Neurology Input
March 2016:
Sinemet trial. Negative trial would indicate
MSA.
Gabapentin Increased.
Neurology Input
May 2016 probable neurodegenerative
disorder possibly MSA
July 2016 - No diagnostic epileptiform
abnormalities on EEG. Mildly slow
background rhythms ?due to medication.
Aug 2016 - Unsuccessful trial of L-dopa
L brachalgia absent L bicep and supinator
Lower cervical cord compression on MRI
Neurosurgery Input
Had cervical spinal surgery anterior
fixation to correct stenosis.
After surgery there was partial improvement
in use of limbs.
Awaiting further neurosurgical input re:?
thinning of the cerebral cortex.
Medical History

In addition to the neurological complaints:


Chronic back pain
Diabetes Mellitus?
Hypertension
Hepatitis C
Bilateral inguinal Hernias
Arthritis
No hx of epilepsy or head trauma
Surgical History
Anterior Fixation of the Cervical Spine as
above.
Current Medications

Diazepam 5mg. po. TDS Olanzapine 5mg po nocte

Sevredol 10mg po Q 6hrly Clopidogrel 75mg po AM

Gabapentin 900mg po TDS Lansoprazole 30mg po AM

Procyclidine 5mg po BD Fresubin one 2kCAl tab po AM

Amlodipine 5mg po AM Tamsulosin MR 400mcg po AM

Venlafaxine 75mg AM/37.5mg PM Finasteride 5mg po AM


Past Medications
Quetiapine
Sertraline
Citalopram
Reboxetine
Levodopa/Carbidopa (Sinemet)
Allergies
PENICILLIN
Family background
Unhappy childhood. His parents separated and his
mother's new partner was abusive. His biological
father eventually returned but died after a few years.

1 of 5 children. There was a family dispute over an


inheritance and client has not spoken to two of his
brothers in a long time. He feels bad that they do not
call to enquire about him since he has fallen ill. He has
one sister and she takes him for a weekend
sometimes to give his wife a respite.

2 niece are diagnosed with Bipolar Affective Disorder


and 1 attempted suicide but did not succeed.
Social History
Married. Wife is very supportive.
No children.
Has a dog he cares for very much.
He was active in the gym and did
kickboxing.
Education/ Occupation
Left school at age 14 to go to work to
support the family.
Poor literacy
Worked in construction/ as a bricklayer in
the past but has not worked/has been
benefits since at least 2008.
Forensic
Had legal trouble in the past for fighting and
drug dealing.
Denied any recent charges/convictions
Mental Status Examination
Normal attire. Normal activity levels. Appeared
confused at times.
Cooperative during the interview.

Mood sad. Affect generally euthymic.

Speech Dysarthritic+++. Slow and soft. Difficult to


assess thought form.

Auditory hallucinations ++ ?visual hallucination.


No obvious delusions.

Deficits noted in memory and cognition.


Physical Examination
Abnormal movements of the mouth and tongue noted.

No primitive reflexed or frontal release signs noted at


the time of the home visit.

However, on a detailed physical examination carried


out in a neurological clinic, frontal release signs has
been recorded as being present eg. Jaw jerk and pout.
Additionally signs of cerebellar dysfunction were
elicited in the neurology clinic which were not
convincingly seen during the examination during the
home visit.

With due respect to all the clinicians involved the


significance of these waxing and waning neurological
signs is unclear.
Management
The decision was taken to admit AL to the
inpatient unit and he agreed to be admitted
informally.
On the ward his mental state fluctuated and
he became confused at times and he tried to
leave the ward and he had to be sectioned.
5/4 then 5/2 then section 2.
Investigations
12.10.17 Carotid Doppler US
unremarkable

ACE III Total Score 51/100


Attention 8/18
Memory9/26
Fluency 3/14
Language 21/26
Visuospatial 10/16
Investigations
FBC, U&E, LFT, TFT, Lipids, Prolactin, Vitamin B12
and Folate WNL
22.09.17 MRI Head with contrast
Moderate global involutional change (more than
expected for age) with mild hippocampal
atrophy
Multiple small foci in deep white matter
consistent with ischemia
No microhemorrhages

27.09.17 MRI cervical spine large disc osteophyte C5


causing mild cord compression
Differential Diagnoses
Dementia ? Aetiology
Vascular/Lewy Body/Alzheimer's/Hep C
Tardive Dyskinesia
Multi System Atrophy
Parkinson's Disease/ Parkinson Plus
Syndrome
Ischemic CVA's
Schizoaffective Illness
Amphetamine Use Disorder ?in remission
DISCUSSION
Dementia
Dementia is a syndrome (a group of related symptoms)
associated with an ongoing decline of brain functioning.
This may include problems with:
memory loss
thinking speed
mental sharpness and quickness
language
understanding
judgement
mood
movement
difficulties carrying out daily activities
Dementia
People with dementia can become apathetic or
uninterested in their usual activities, or may
have problems controlling their emotions.
They may also find social situations challenging
and lose interest in socialising. Aspects of their
personality may change.
A person with dementia may lose empathy
(understanding and compassion), they may see
or hear things that other people do not
(hallucinations).
Dementia
Because people with dementia may lose the
ability to remember events or fully understand
their environment or situations, it can seem as if
they're not telling the truth, or are wilfully
ignoring problems.
As dementia affects a person's mental abilities,
they may find planning and organising difficult.
Maintaining their independence may also
become a problem.
A person with dementia will therefore usually
need help from friends or relatives, including
help with decision making.
Hepatitis C and Dementia
HCV infection is considered a systemic disease
because of involvement of other organs and tissues
concomitantly with liver disease.
Among the extrahepatic manifestations,
neuropsychiatric disorders have been reported in up to
50% of chronic HCV infected patients.
Both the central and peripheral nervous system may
be involved.
Main HCV-associated neurological conditions include
cerebrovascular events, encephalopathy, myelitis,
encephalomyelitis, and cognitive impairment
Hepatitis C and Dementia
Brain fog, depression, anxiety, and fatigue are at the
top of the list of psychiatric disorders.
Moreover, HCV infection is known to cause both motor
and sensory peripheral neuropathy in the context of
mixed cryoglobulinemia, and has also been recently
recognized as an independent risk factor for stroke.
These extrahepatic manifestations are independent of
severity of the underlying chronic liver disease and
hepatic encephalopathy.

Adinolfi LE et al. HCV and neuropsychiatric diseases. World J Gastroenterol


2015 February 28; 21(8): 2269-2280
Hepatitis C and Dementia
The brain is a suitable site for HCV replication,
where the virus may directly exert neurotoxicity;
Other mechanisms proposed to explain the
pathogenesis of neuropsychiatric disorders in
chronic HCV infection include:
Derangement of metabolic pathways of infected
cells,
alterations in neurotransmitter circuits,
autoimmune disorders, and
cerebral or systemic inflammation.
Hepatitis C and Dementia
A pathogenic role for HCV is also suggested by
improvement of neurological and psychiatric
symptoms in patients achieving a sustained
virologic response following interferon
treatment.
Hepatitis C and Dementia
In chronic HCV infection, cerebrovascular acute
and chronic events have been reported with a
higher prevalence than that observed in the
general population.

Several studies have reported heterogeneous


neuropsychological deficits in chronic HCV
infected patients, including inadequate
concentration and working memory speed,
impaired ability of sustained attention,
decreased psychomotor speed.
Hepatitis C and Dementia
Failure in domains depending upon front
striatal systems, including fine motor speed,
learning and information processing efficiency,
may underlie neurocognitive disorders.
An association between HCV and impairment of
a range of executive functions, including
reasoning, abstraction, mental flexibility and
verbal response inhibition has also been
described.
Hepatitis C and Dementia
While interferon- treatment itself is known to
possibly determine neuropsychiatric side
effects, on the other hand, the drug ability to
improve neurological and psychiatric symptoms
in HCV patients achieving a sustained virologic
response (SVR) has been frequently reported in
the literature.
Patients achieving a SVR have been shown to
display reduced brain inflammation and
improved neuropsychological functions,
including verbal learning, memory, and visual-
spatial memory.
Thank you for your attention.

Questions?

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