Case presentation presented at the teaching session at Royal Glamorgan Hospital in Wales. It gives a case history of a patient then is followed by a discussion of Dementia in general and Hepatitis C Demential in more detail
Case presentation presented at the teaching session at Royal Glamorgan Hospital in Wales. It gives a case history of a patient then is followed by a discussion of Dementia in general and Hepatitis C Demential in more detail
Case presentation presented at the teaching session at Royal Glamorgan Hospital in Wales. It gives a case history of a patient then is followed by a discussion of Dementia in general and Hepatitis C Demential in more detail
Case presentation presented at the teaching session at Royal Glamorgan Hospital in Wales. It gives a case history of a patient then is followed by a discussion of Dementia in general and Hepatitis C Demential in more detail
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.