APPLE ONE BROKENSHIRE MEDICAL CORPORATION

DEPARTMENT OF INTERNAL MEDICINE

END-ROTATION CASE PRESENTATION

JULY 31, 2022

CASE PROTOCOL

PRESENTORS:

PGI Cano, Mikaela Jessica Victoria D.

PGI Madianda, Jan Recarlo R.

PGI Mohanty, Anica Serbina G.

PGI Teves, Johnna

MODERATOR:

Dr. Earl J. Niervo

Objectives

1. To present a case of Mixed Dementia, Alzheimer’s Disease and Vascular Dementia

2. To discuss the history, physical examination, and management of a patient with the
above conditions
3. At the end of this discussion, the readers will be able to:
a. Recognize pertinent signs and symptoms of the above conditions
b. Manage accordingly
General Data

Name : L.E
Age : 69 years old
Address : Polomolok, South Cotabato
Birthdate :
Religion : Catholic
Admission Date : July 13, 2022
Admission Time :
Reliability :

Chief Complaint: Increased Sleeping Time

History of Present Illness

4 years PTA, onset (+) episodes of forgetfulness associated with episodes of disorganized
behavior such as passing urine at random areas at home, initially tolerated condition until,

3 years PTA Patient had trauma to the head hitting his occipital area to a cabinet, sustained soft
tissue contusion and had loss of consciousness and was brought to a local hospital, upon
regaining consciousness, pt had slurred speech and difficulty obeying commands and right
sided weakness and was then referred to another hospital and was admitted at the ICU for
approximately 1 month where ct scan and mri was done. Patient underwent regular PT sessions
upon discharge and noted improvement of motor deficits and was able to ambulate with a
walker. However during the pandemic, patient was lost to follow up, rehab sessions were
discontinued and maintenance medications continued.

In the Interim, Patient was observed to have increased sleeping time, difficulty obeying
commands, noted to be aphasic since last year and noted worsening of weakness hence family
opted to seek consult and do further work ups hence admission.

Past Medical History

● (+) DM Jan 2019
● (+) CVA with right sided weakness Jan 2019 with the ff meds:
○ 1. Memantine 10mg tab OD
○ 2.conzace tab OD
○ 3.Baclofen 10mg tab OD
○ .Levetiracetam 500mg/tab, 1/2 tab BID
○ Sitagliptin/Metformin 50/500 tab OF
○ Clopidogrel 75mg/tab OD
○ Digoxin 0.25mg/tab, 1/2 tab OD
 ● (-) BA
● (-) prev consults prior to 2019
● (-)FDA
● JUNE 2019- PTB treated x 6 mos

Personal and Social History

● (+) Previous Occasional Beverage Drinker
● (-) Smoker
● Previously works as an Engineer
● Fully Vaccinated: Sinovac x 2 doses, No booster

Family Medical History

● (+) Arthritis - Paternal
● (+) DM, HPN - Maternal/Paternal

Review of Systems

General: (-) Weightloss, (-) Fatigue, (-) Fever, (+) Weakness

Head: (-) Headache
Skin (-) Mass/Lesions, (-) HYperpigmentation, (-) Jaundice, (-) Cyanosis
Neck: (-) Mass/Lesions, (-) Tenderness, (-) Rigidity/ Stiffness
Chest & Lungs: (-) Chest Pain, (-) DYspnea, (-) Orthopnea, (+) Chronic Productive Cough w/
whitish sputum
Cardiac: (-) Edema, (-) Palpitations
Gastrointestinal: (-) Vomiting, (-)Hematemesis, (-) Hematochezia, (-) DIarrhea, (-) ABdominal
DIstention, (-) Loose Bowel Movement
Genito Urinary: (-) dysuria, (-) Oliguria

Physical Examination

Awake, Comfortable, Not in Respiratory Distress

Anicteric Sclerae, Pink Palpebral Conjunctiva, Isocoric pupils equally reactive to light, (-) neck
rigidity
Equal Chest Expansion, Clear Breath Sounds, (-)crackles
Distinct Heart Sounds, Irregularly Irregular rate and rhythm
Flabby abdomen, soft non tender
full pulses, no edema

Neurologic Examination

Patient is aphasic, unable to obey commands, no spontaneous eye opening upon examination
but resists opening of eyes.

CN I - not assessed
CN II-III - both pupils equally reactive to light at 3-4mm
CN III, IV, VI - unable to assess
CN VII – (+) right sided facial asymmetry
CN VIII - unable to assess
CN IX, X - unable to assess, able to tolerate solid food
CN XI - unable to assess
CN XII - unable to assess

Motor:
RIGHT LEFT

Spastic w/
UPPER 4/5
contracture

LOWER 3/5 4/5

Negative Kernig’s sign and Brudzinski's sign

Salient Features

Pertinent Positives Pertinent Negatives

65 years old No Chest Pain

Male No Dyspnea
Increased Sleeping TIme No Orthopnea
(+) generalized body weakness No Fever
DIfficulty Obeying Commands No Dysuria
Aphasic No urinary retention/ incontinence
No spontaneous eye opening No Nausea/ Vomiting
Motor RUE: Spastic, RLQ: 3/5, LE: 4/5 No Loose Bowel Movement
Right Sided Facial Asymmetry No Headache
3 years PTA, Trauma to Occipital Part of the No neck rigidity
Head with soft tissue contusion and LOC Negative Kernig’s sign and Brudzinski's sign
4 years PTA (+) Episodes of Forgetfulness,
episodes of disorganized behavior such as
passing urine at random place at home.
(+) CVA w/ Right Sided Weakness on Jan
2019
(+) Diabetes Mellitus
(+) Chronic Cough with Whitish Sputum
History of PTB 2019 - treated

Differential Diagnoses

1. ALZHEIMER’S DISEASE
 Alzheimer’s disease is the most common cause of dementia, contributing to an
estimated 60-70% of all cases. This disease can manifest as early as the third decade of
life, but it is the most common cause of dementia in the elderly. In typical amnestic AD,
brain atrophy begins in the median temporal lobes before spreading to the inferior
temporal, lateral, medial, parietal and dorsolateral frontal cortices. Microscopically, there
are widespread neuritic plaques containing amyloid beta, neurofibrillary tangles and
amyloid beta accumulation in blood vessel walls in the cortex and leptomeninges.

RULE IN RULE OUT

- Elderly patient (65 years old) - No family history of alzheimer’s

- Patient is a diabetic (diabetes disease
increases the risk of AD 3 fold) - Cannot be fully ruled out
- (+) episodes of forgetfulness
- (+) episodes of disorganized
behavior such as passing urine at
random place at home.
- (+) Increased Sleeping TIme
- Aphasia
- Motor RUE: Spastic, RLQ: 3/5, LE:
4/5

2. FRONTOTEMPORAL DEMENTIA
Frontotemporal dementia is considered a disease of abnormal protein aggregation with
either tau or transactive response DNA binding protein.

RULE IN RULE OUT

- Elderly patient (65 years old) - No emotional and social

- Aphasia dysfunction such as apathy,
- (+) Increased Sleeping TIme disinhibition, compulsivity, loss of
empathy and overeating

3. CHRONIC MENINGITIS
Chronic meningitis is diagnosed when a characteristic neurological symptom exists for >
4 weeks associated with a persistent inflammatory response in the CSF. Most common
cases of chronic meningitis are caused by meningeal infections, malignancy,
autoimmune inflammatory disorders, chemical meningitis and parameningeal infections.

RULE IN RULE OUT

- Increased Sleeping TIme - No fever

 - DIfficulty Obeying Commands - No headache
- Aphasic - No neck rigidity
- (+) generalized body weakness - No double vision
- No spontaneous eye opening - Negative Kernig’s sign and
- Motor RUE: Spastic, RLQ: 3/5, LE: Brudzinski's sign
4/5 - No radiculopathies (numbness in
arms and legs)
- No ataxia
- No urinary retention/ incontinence

4. METABOLIC ENCEPHALOPATHY
Metabolic encephalopathies comprise neurological disorders not caused by primary
structural abnormalities rather they result from systemic illness such as diabetes, liver
diseases, renal failure and heart failure.

RULE IN RULE OUT

- Elderly patient (65 years old) - No delirium

- Patient is a diabetic - No jaundice
- Increased Sleeping TIme - No nausea vomiting
- DIfficulty Obeying Commands - No Chest Pain
- Aphasic - No Dyspnea
- (+) episodes of forgetfulness - No Orthopnea
- (+) generalized body weakness - No Dysuria
- (+) episodes of disorganized - No urinary retention/ incontinence
behavior - No Nausea/ Vomiting
- No spontaneous eye opening - No Loose Bowel Movement
- Motor RUE: Spastic, RLQ: 3/5, LE: - No seizures
4/5 - No tremors
- No visual changes/ symptoms

5. VASCULAR DEMENTIA
Vascular dementia is a subset of dementia cases due primarily to one or more
symptomatic strokes and is usually ranked the second most frequent cause of dementia.

RULE IN RULE OUT

- 65 years old - Cannot be ruled out

- Male
- Increased Sleeping TIme
- (+) generalized body weakness
- DIfficulty Obeying Commands
- Aphasic
 - No spontaneous eye opening
- Motor RUE: Spastic, RLQ: 3/5, LE:
4/5
- Right Sided Facial Asymmetry
- (+) trauma to Occipital Part of the
Head with soft tissue contusion
and LOC
- (+) Episodes of Forgetfulness
- (+) episodes of disorganized
behavior
- (+) CVA w/ Right Sided Weakness
on Jan 2019

Admitting Impression

Vascular Dementia, S/P CVA infarct- Cardioembolic with Right Sided Residual Weakness and
Aphasia (2019), Cardiac Dysrhythmia: AF in MVR Type 2 Diabetes Mellitus, PTB treated 2021

Course in the ER/Ward

HD 1 Admit
Secure Consent to care
VS every 4 hours, include NVS
I & O every Shift
Diet: DM Diet with SAP at 1600 kcal in 3 full meals and 2 snacks
IVF: PNSS 1L to run at 60cc/hr
Diagnostics:
CBC, Chest Xray, S. ELectrolytes, Creatinine, Hba1c, Lipid Profile, SGPT, UA,
SUA, 2d- Echo, CBG every 6 hours pre meals
Medications:
a. Memantine 10mg tab OD
b. Conzace tab OD
c. Baclofen 10mg tab OD
d. Levetiracetam 500mg/tab, ½ tab BID
e. Sitagliptin/Metformin 50/500mg tab OD
f. Clopidogrel 75 mg/tab OD
g. DIgoxin 0.25mg/tab ½ tab OD
h. Atorvastatin 40mg tab ODHS
NEURO Plans
For Cranial MRI (Dementia Protocol)
Final Diagnosis

Mixed Dementia, Alzheimer’s Disease and Vascular Dementia

Type 2 Diabetes Mellitus
Hypertensive Cardiovascular Disease, Left Ventricular Hypertrophy, Atrial Fibrillation in
Moderate Ventricular Response, Not in failure

CASE DISCUSSION

Dementia is a disorder characterized by a decline in cognitive function with a severity

that interferes with daily functioning. The most common cause of dementia is Alzheimer’s
Disease, caused by the deposition of neurofibrillary tangles and senile plaques in the brain,
followed by Vascular dementia, caused by ischemic injury to the brain.

ALZHEIMER’S DISEASE
Alzheimer’s Disease (AD) is a neurodegenerative disease characterized by an insidious
onset and progressive impairment of both behavioral and cognitive functions. The cognitive
decline in AD involves the impairment of memory, comprehension, communication,
concentration, and judgment.

Epidemiology
Among the risk factors for AD, the most important are age of >70 years old and a
positive family history of AD. The prevalence increases with each decade of adult life. Other risk
factors include the female sex, history of head trauma, and low educational attainment.

Clinical Manifestations and Natural Course of Illness

There is a characteristic pattern in the cognitive decline of AD beginning with memory
impairment, language and visual spatial deficits, and eventually executive dysfunction. Some
patients may also initially present with visual processing dysfunction or a progressive aphasia
with difficulties in naming and repetition before progressive to other cognitive domains.

Initially, in the early stages of typical amnestic AD, the decline in memory may simply be
attributed to the usual forgetfulness of aging. As the disease progresses, the memory loss
becomes pronounced enough and is now termed mild cognitive impairment, with 50% of
patients progressing to AD over 4 years. Eventually, cognitive impairment will interfere with daily
living, with some patients even getting lost during walks or commutes. Changes in the
environment could serve as triggers for the destabilization of the patient. Anosognosia, or the
patient's unawareness of their own difficulties, may be seen.
 During the middle stages, patient now requires daily supervision as they will be unable to
work or tend for themselves and are easily confused. Language impairment begins as difficulty
naming until fluency is eventually impaired. Apraxia, trouble performing learned sequential
motor tasks, is seen.

In the late stages, loss of judgment and reasoning are prominent, as are simple
delusions and disinhibitions. Nighttime wandering may become an issue given the disruption in
sleep-wake patterns. As the patients enter the end stages of AD, they become rigid, mute,
incontinent, and bedridden. Death typically results from malnutrition, secondary infection,
emboli, or especially aspiration. The course of disease ranges from 1 to 25 years.

VASCULAR DEMENTIA
Vascular dementia denotes cognitive and behavioral deficits that are associated with
cerebrovascular disease (CVD). This results when CVD is severe enough to cause deficits in
occupational, social, or functional abilities. Vascular disease can disrupt structural cognitive
networks with infarcts, bleeds, chronic progressive white matter degeneration, and altered
cerebral hemodynamics.

Epidemiology
The strongest risk factor for vascular dementia is the same as that of CVD and stroke:
age. Other risk factors are chronic hypertension, hyperlipidemia, diabetes, and smoking. Atrial
fibrillation or heart failure can cause cognitive impairment via embolic infarcts and hypoxemia.
Post-stroke dementia risk factors overlap with those identified for AD, such as those mentioned
above.

Clinical Manifestations and Pathophysiology

Cognitive impairment in vascular dementia occurs in a stepwise progression, especially with
multi-infarct dementia. Vascular dementia is strongly associated with hemorrhagic and ischemic
strokes, with an estimated one third of stroke survivors affected by post-stroke dementia. With
hemorrhagic strokes, the disruption of cerebral networks will depend on the size and location.
Subarachnoid hemorrhages have the highest chance of developing dementia syndrome. This is
a result of vessel wall damage and inflammation. Ischemic strokes cause neurobehavioral
symptoms as a function of cerebral lesion size and location, including aphasia, apraxia,
agnosia, and inattention. Some ambiguity may exist between location and symptoms as a result
of the interconnected nature of the brain as well as the sequences of cerebral inflammation and
blood-brain barrier disruption caused by strokes. Chronic cerebral small vessel disease shows
the strongest life association with vascular dementia. This causes occlusion of the deep
penetrating arteriolose and disease of the draining vessels, causing damage to the subcortical
structures such as basal ganglia, thalami, and white matter infarcts. Large lesions or lacunar
infarcts can result in a stepwise or gradual decline in cognition. Concurrent CVD lowers the
threshold for dementia due to AD.
Diagnostics

Evaluation of possible dementia requires a brief medical history and a cognitive and neurologic
examination. The history remains the most important diagnostic tool and should be obtained
from both the patient and a close family member or friend. While some patients complain of
forgetfulness, others are unable to recall details of their history and in some instances have
anosognosia.

One clue that a patient has a memory problem occurs when the person accompanying them
provides the medical history. History should characterize the nature, magnitude, and course of
cognitive changes. Nature refers to the cognitive domains affected. Is there loss of episodic
memory, or language abilities? The magnitude refers to the severity: does the cognitive loss
affect daily functions, such as the patient’s ability to manage her own affairs? Is the course with
an insidious onset and a slow progression or a rapid onset and fluctuating and stepwise
progression? The history should focus on medical conditions that could affect cognition
including vascular disease risk factors, existing brain conditions, and use of medications that
can impair cognition. A family history might identify young-onset dementia (onset in persons
younger than 65 years) in first-degree relatives, suggesting one of the rare inherited genetic
forms of dementia.
Management and Treatment

Alzheimer’s Disease (AD)

The management of AD is challenging and gratifying despite the absence of a cure or a robust
pharmacologic treatment. The primary focus is on long-term amelioration of associated
behavioral and neurologic problems, as well as providing caregiver support.

Building rapport with the patient, family members, and other caregivers is essential. In the early
stages of AD, memory aids such as notebooks and posted daily reminders can be helpful.
Family members should emphasize activities that are pleasant while curtailing those that
increase stress on the patient. Kitchens, bathrooms, stairways, and bedrooms need to be made
safe, and eventually patients will need to stop driving. Loss of independence and change of
environment may worsen confusion, agitation, and anger. Communication and repeated calm
reassurance are necessary. Caregiver “burnout” is common, often resulting in nursing home
placement of the patient or new health problems for the caregiver. Respite breaks for the
caregiver help to maintain a successful long-term therapeutic milieu. Use of adult day care
centers can be helpful. Local and national support groups, such as the Alzheimer’s Association
and the Family Caregiver Alliance, are valuable resources. Internet access to these resources
has become available to clinicians and families in recent years.

Donepezil (target dose, 10 mg daily), rivastigmine (target dose, 6 mg twice daily or 9.5-mg patch
daily), galantamine (target dose 24 mg daily, extended-release), and memantine (target dose,
10 mg twice daily) are approved by the U.S. Food and Drug Administration (FDA) for the
treatment of AD. Due to hepatotoxicity, tacrine is no longer used. Dose escalations for each of
these medications must be carried out over 4–6 weeks to minimize side effects. The
pharmacologic action of donepezil, rivastigmine, and galantamine is inhibition of the
cholinesterases, primarily acetylcholinesterase, with a resulting increase in cerebral
acetylcholine levels.

Memantine appears to act by blocking overexcited N-methyl-d-aspartate (NMDA) glutamate

receptors. Double-blind, placebo-controlled, crossover studies with cholinesterase inhibitors and
memantine in moderate to severe AD have shown them to be associated with improved
caregiver ratings of patients’ functioning and with an apparent decreased rate of decline in
cognitive test scores over periods of up to 3 years. The average patient on an
anticholinesterase inhibitor maintains his or her mini-mental state examination (MMSE) score for
close to a year, whereas a placebo-treated patient declines 2–3 points over the same time
period. Memantine, used in conjunction with cholinesterase inhibitors or by itself, slows
cognitive deterioration and decreases caregiver burden for patients with moderate to severe AD,
but is not approved for mild AD. Each of these compounds has only modest efficacy for AD.
Cholinesterase inhibitors are relatively easy to administer, and their major side effects are
gastrointestinal symptoms (nausea, diarrhea, cramps), altered sleep with unpleasant or vivid
dreams, bradycardia (usually benign), and muscle cramps.

Vascular Dementia (VaD)

Treatment of VaD must be focused on accurate diagnosis of VaD so that new ischemic injury
can be prevented by stabilizing or removing the underlying causes. Effective control of
modifiable risk factors, including hypertension, smoking, alcohol intake, sodium consumption,
diabetes mellitus, obesity, and the metabolic syndrome, are key to slowing the rising global
prevalence of this condition. There is a great need for sensitive and specific in vivo biomarkers
of VCI-VaD for early diagnosis and ultimately a surrogate marker of therapeutic efficacy in
clinical trials.

References:
Harrison’s Principles of Internal Medicine 21st Ed.

Arvanitakis Z, Shah RC, Bennett DA. Diagnosis and Management of Dementia: Review. JAMA.
2019 Oct 22;322(16):1589-1599. doi: 10.1001/jama.2019.4782. PMID: 31638686; PMCID:
PMC7462122.