Approach to gradual cognitive decline: Clinical sciences

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Approach to gradual cognitive decline: Clinical sciences

Internal Medicine

Internal Medicine

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Acute stroke (ischemic or hemorrhagic) or TIA: Clinical sciences
Cardiovascular disease screening: Clinical sciences
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Peripheral arterial disease and ulcers: Clinical sciences
Approach to gradual cognitive decline: Clinical sciences
Alzheimer disease: Clinical sciences
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Delirium: Clinical sciences
Vitamin B12 deficiency: Clinical sciences
Approach to mood disorders: Clinical sciences
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Septic arthritis: Clinical sciences
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Stevens-Johnson syndrome and toxic epidermal necrolysis: Clinical sciences
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Toxic shock syndrome: Clinical sciences
Approach to hematochezia: Clinical sciences
Hemorrhoids: Clinical sciences
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Approach to headache or facial pain: Clinical sciences
Idiopathic intracranial hypertension: Clinical sciences
Primary headaches (tension, migraine, and cluster): Clinical sciences
Approach to joint pain and swelling: Clinical sciences
Calcium pyrophosphate deposition disease (pseudogout): Clinical sciences
Gout: Clinical sciences
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Psoriatic arthritis: Clinical sciences
Reactive arthritis: Clinical sciences
Approach to knee pain: Clinical sciences
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Approach to nosocomial infections: Clinical sciences
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Basal cell carcinoma: Clinical sciences
Benign skin lesions: Clinical sciences
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Lipoma: Clinical sciences
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Approach to syncope: Clinical sciences
Approach to unintentional weight loss: Clinical sciences
Approach to vomiting (acute): Clinical sciences
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Approach to abdominal wall and groin masses: Clinical sciences
Acid-base map and compensatory mechanisms
Physiologic pH and buffers
Acid-base disturbances: Pathology review
Buffering and Henderson-Hasselbalch equation
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Decision-Making Tree

Transcript

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Gradual cognitive decline refers to the slow and progressive cognitive impairment that can affect memory, behavior, personality, organizational and decision-making skills, and visuospatial awareness. It can occur due to various neurologic conditions, including brain tumors, normal pressure hydrocephalus, Huntington disease, and different types of dementia.

Now, if a patient presents with gradual cognitive decline, you should obtain a focused history and physical exam. You should also obtain cognitive screens, such as the Montreal Cognitive Assessment or Mini-Mental State Examination. Also, be sure to perform a depression screen because depression can sometimes present as cognitive impairment, which is also known as pseudodementia.

History typically reveals memory difficulties, like forgetting important appointments; behavior or personality changes, such as aggressiveness or impulsivity; and difficulties with organization and completing tasks, known as loss of executive function. History might also reveal difficulty with visuospatial tasks, such as parking or using the stairs, resulting in accidents. In addition, there might be a family history of cognitive decline.

Depending on the underlying cause and the stage of the disease, the physical exam may or may not be normal. On the flip side, the cognitive screen, which includes testing short-term memory, language, attention, and visuospatial skills, will be abnormal. Lastly, the depression screen will be negative, but keep in mind that many patients with cognitive impairment will also have a mood disorder. With these findings, diagnose cognitive impairment.

Now, here’s a clinical pearl! Some metabolic conditions, including hypothyroidism and vitamin B12 deficiency, can cause cognitive impairment, so the initial evaluation should also include labs, like thyroid stimulating hormone and vitamin B12 levels.

Time for a high-yield fact! If your patient has depressive symptoms prior to their cognitive decline, such as sad, depressed, or hopeless mood, lack of energy and motivation, and flat or tearful affect, think of pseudodementia. This is very important as pseudodementia is reversible and should be treated as a depressive disorder. In this case, you’ll probably need to refer your patient for psychotherapy and prescribe an antidepressant, typically a selective serotonin reuptake inhibitor.

Alright, once you diagnose cognitive impairment, obtain brain imaging with a CT or MRI. Next, assess imaging findings and determine if there are any abnormalities other than brain atrophy.

If there are additional abnormalities, look for the presence of mass lesion. If you find it, diagnose a tumor as the likely cause of the cognitive impairment. Patients with tumors in the frontal or temporal lobes would be particularly at risk for cognitive impairment. Depending on the location of the tumor, they might also present with other signs and symptoms, like hemiparesis and seizures.

On the other hand, if there are imaging abnormalities but no mass lesion present, you should think of normal pressure hydrocephalus, vascular dementia, and HIV-associated neurocognitive disorder.

First, let’s focus on normal pressure hydrocephalus. In this case, the patient reports progressive difficulty with walking and urinary symptoms, such as urinary urgency and frequency, or in some cases, urinary incontinence.

On physical exam, you’ll notice significant gait abnormalities. In normal pressure hydrocephalus, the gait is slow, with small steps and a wide base. Additionally, the patient has difficulty with turns, taking multiple steps to turn around. They might have gait apraxia, which is described as a magnetic gait because the feet look stuck to the ground as the patient shuffles around. Lastly, perform a pull test to test postural stability. To do this, stand behind the patient and suddenly pull back on their shoulders. Individuals who can maintain their balance will either not take any steps backwards or, at most, take one to two steps back. However, individuals with normal pressure hydrocephalus have postural instability, meaning they will take multiple small steps backwards, and might even fall. In that case, the pull test is positive.

Finally, imaging reveals ventriculomegaly with minimal cortical atrophy and no evidence of CSF obstruction. With these findings, consider normal pressure hydrocephalus and perform a lumbar puncture. If the lumbar puncture demonstrates a normal opening pressure, diagnose normal pressure hydrocephalus.

Here's a clinical pearl! Management of normal pressure hydrocephalus includes consideration of a permanent CSF shunt placement, such as a ventriculoperitoneal shunt, which can potentially improve cognition and gait.

Alright, now let’s take a look at vascular dementia. These patients have a medical history of cardiovascular risk factors such as hypertension, hyperlipidemia, diabetes, coronary artery disease, atrial fibrillation, and tobacco use. Also, history will reveal multiple previous strokes. The patient or a loved one will describe that cognitive decline is occurring in a stepwise fashion that seems to correlate with the timing of prior strokes.

On the physical exam, you’ll typically notice focal neurologic deficits, such as visual field loss, weakness, or aphasia. Also, you might note high blood pressure or an irregular heart rate. Finally, if the imaging shows multiple infarcts and extensive white matter microvascular disease, diagnose vascular dementia.

Next, let’s focus on HIV-associated neurocognitive disorder. Here, history reveals a known HIV infection. The patient may or may not be compliant with highly active antiretroviral therapy. Their exam might demonstrate sensory loss in the distal limbs consistent with peripheral neuropathy. You might also notice other signs of HIV-related conditions, such as oral candidiasis and lesions from Kaposi sarcoma.

Sources

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