How to differentiate between types of dementia

Learn about the seven common causes of dementia, and the signs and symptoms that differentiate these conditions.
Last update7th Jan 2021

Now that you know how to identify dementia, let’s discuss several common causes of dementia. There are seven diseases and conditions that can cause dementia-like symptoms:

  1. Alzheimer’s disease
  2. Frontotemporal dementia
  3. Tumors
  4. Chronic subdural hematoma
  5. Normal pressure hydrocephalus
  6. Vitamin B12 deficiency
  7. Creutzfeldt-Jakob disease

Alzheimer’s disease

Alzheimer’s disease is the most common cause of dementia worldwide. Patients often present with significant short-term memory difficulties, social withdrawal, and depression. Initially, language and motor functions are generally preserved.

Figure 1. Symptoms of Alzheimer’s disease include short-term memory difficulties, social withdrawal, and depression.

As Alzheimer’s disease progresses over the next two to ten years, the patient becomes increasingly confused and incapable of managing their own affairs. There may be significant behavioral difficulties and psychomotor retardation associated with the disease progression. The patient’s functions generally deteriorate to the point where constant care and supervision is needed. Life expectancy from the time of diagnosis is generally eight to ten years.

Figure 2. As the disease progresses, patients with Alzheimer’s disease experience increased confusion, behavioral difficulties, and the need for constant care.

Management of Alzheimer’s disease

To manage the progressive symptoms, initiate cholinesterase inhibitors in your patients with Alzheimer’s disease. While these medications often help with symptoms of Alzheimer’s disease, they have not been shown to alter the course of the disease. Cholinesterase inhibitor medications include donepezil, galantamine, and rivastigmine.

N-methyl-D-aspartate antagonists such as memantine may benefit patients with moderate to severe Alzheimer’s disease. When appropriate, also consider the use of antidepressants, anti-anxiety agents, and antipsychotics in the care of your patients with Alzheimer’s disease.

Regular and relatively vigorous exercise alongside a Mediterranean-like diet may help slow disease progression and delay onset in vulnerable patients.

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Frontotemporal dementia

Frontotemporal dementia generally occurs in younger patients in the 45- to 65-year-old range. Early on, it may involve significant apathy, behavioral changes, loss of executive functions, and processing difficulties. Frontotemporal dementia often affects speech generation but leaves speech reception intact. Unfortunately, death usually occurs within two to ten years of the diagnosis.

Figure 3. Early symptoms of frontotemporal dementia include significant apathy, behavioral changes, loss of executive functions, processing difficulties, and speech generation difficulties.

Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans can help differentiate frontotemporal dementia from Alzheimer’s disease. As well, MRI should show significant frontotemporal cortical and fronto-insular atrophy.


Tumors can cause dementia-like syndromes. A progression of dysfunction may unfold over just a few months with rapidly growing intrinsic tumors such as glioblastomas. Benign extra-axial tumors (such as meningiomas) may result in a slow and subtle progression of cognitive dysfunctions, particularly with tumors affecting the frontal lobes. With frontal lobe lesions, no other deficits may be detected other than cognitive impairment.

Depending on the location, a tumor can be associated with focal neurological findings such as aphasia, hemianopsia, and hemiparesis. However, neurological findings may also be non-focal. Look for papilledema on an exam, which signifies increased intracranial pressure.

Figure 4. Papilledema in a patient presenting with dementia-like symptoms signifies increased intracranial pressure, which could be a sign of an underlying brain tumor.

While patients with intrinsic tumors (such as gliomas) will not likely show improvements in cognitive deficits with surgical resection, patients with benign extra-axial tumors (such as meningiomas) can show remarkable improvements in cognition after surgery. Keep in mind that the improvement is generally measured over many months.

Chronic subdural hematoma

Chronic subdural hematomas can also lead to dementia-like symptoms. Patients with chronic subdural hematomas often show a relatively rapid progression of dysfunction (on the order of days to weeks). The pathological process is often mistaken for Alzheimer’s disease.

Often, the patient will have sustained a mild to moderate head trauma weeks before they present. However, many patients have no memory of any definitive head trauma.

Some degree of focal neurological findings, such as hemiparesis or aphasia, are also often present. But, cognitive decline may be the only finding. Computed tomography (CT) or MRI can easily make the diagnosis of a subdural hematoma.

Figure 5. Hemiparesis and aphasia may be present with a patient suffering from dementia-like symptoms due to a chronic subdural hematoma.

Chronic subdural hematomas are very treatable, even in debilitated patients. A hematoma consists of liquified blood that can be drained through small drill holes in the skull (with or without anesthesia). If a hematoma is discovered and addressed efficiently, cognitive function can be improved to its baseline status.

Patients who have had chronic subdural hematomas in the past are prone to recurrences. Make sure to assess the patient’s gait function and fall risk after surgery. As well, try to avoid anticoagulants and antiplatelet medications.

Normal pressure hydrocephalus

Normal pressure hydrocephalus (NPH) often presents with the triad of memory loss / cognitive dysfunction, gait difficulties (magnetic gait featuring slow steps and feet that appear to be sticking to the ground), and urinary incontinence.

Figure 6. Memory loss / cognitive dysfunction, gait difficulties, and urinary incontinence are common symptoms in patients suffering from dementia-like symptoms due to normal pressure hydrocephalus (NPH).

In a patient with NPH, non-contrast CT or MRI will reveal significantly enlarged ventricles. This should be out of proportion to any cerebral atrophy.

Patients with NPH will sometimes respond quite nicely to the placement of a ventriculoperitoneal shunt, at about a 50% response rate. Unfortunately, many elderly patients have enlarged ventricles due to surrounding brain volume loss through atrophy. These patients do not have NPH and will not respond to shunting. Unfortunately, the two syndromes are difficult to differentiate clinically.

Patients with suspected NPH are often tested by the removal of cerebrospinal fluid (CSF) through a lumbar puncture or temporary drain placement. The purpose of this test is to look for improvement in function before committing to a surgical shunt placement. Shunting is not risk-free; hematomas, shunt failure, shunt infection, and over-drainage are unfortunately common.

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Vitamin B12 deficiency

Dementia may also result from a vitamin B12 deficiency. Patients with a vitamin B12 deficiency often present similarly to those with NPH (e.g., memory loss, gait disturbance, and urinary incontinence), but tend to also have profound proprioceptive loss, imbalance, and spasticity.

Figure 7. Symptoms that are common with vitamin B12 deficiency, which can mimic dementia, include memory loss, gait disturbances, urinary incontinence, proprioceptive loss, imbalance, and spasticity.

The presence of macrocytic anemia on a complete blood count test may suggest the B12 deficiency. Magnetic resonance imaging of the brain may be unimpressive, but MRI of the spinal cord might show an abnormal signal in the posterior spinal cord. Serum B12 testing, of course, will clinch the diagnosis of this very treatable condition.

Creutzfeldt-Jakob disease

Creutzfeldt-Jakob disease (CJD) is a rare and untreatable disease caused by prions. Prions are non-living proteins that fold into abnormal shapes and somehow induce normal proteins in the brain to do the same. They are responsible for several rare diseases—including CJD.

Creutzfeldt-Jakob disease presents with rapidly progressive cognitive deficits, ataxia, and myoclonus. Generally, the dementia progresses over months without any structural pathology on MRI.

Figure 8. Symptoms of Creutzfeldt-Jakob disease (CJD), which also causes dementia-like symptoms, include cognitive deficits, ataxia, and myoclonus.

If CJD is suspected, a lumbar puncture is often performed to look for 14-3-3 proteins in the CSF. As well, an electroencephalogram (EEG) may show a characteristic pattern for the disease, including frontal rhythmic delta activity and periodic sharp wave complexes.

On rare occasions, a brain biopsy is pursued. However, brain biopsies for patients with CJD are problematic because the disease has been transmitted through contaminated surgical equipment—despite standard decontamination procedures.

Unfortunately, there is no effective treatment for CJD. Death usually occurs within a year of diagnosis.

It is important to remember that all of the diseases and conditions discussed here can cause dementia-like symptoms. Even though Alzheimer’s disease is the most common cause of dementia, it is important to rule out differential diagnoses.

That’s it for now. If you want to improve your understanding of key concepts in medicine, and improve your clinical skills, make sure to register for a free trial account, which will give you access to free videos and downloads. We’ll help you make the right decisions for yourself and your patients.

Recommended reading

  • Dementia care central. 2020. Mini-mental state exam (MMSE) Alzheimer’s / dementia test: Administration, accuracy and scoring.
  • Dementia Care Central. 2020. Mini-mental status examination.
  • Huang, A. Cognitive screening toolkit.
  • Kumar, A, Singh, A, and Ekavali. 2015. A review on Alzheimer’s disease pathophysiology and its management: an update. Pharmacol Rep67: 195–203. PMID: 25712639
  • Lakhan, SE. 2019. Alzheimer disease. Medscape
  • Louis, ED, Mayer, SA, and Rowland, LP. 2015. Merritt’s Neurology. 13th edition. Philadelphia: Wolters Kluwer.
  • Mayeux, R. 2010. Clinical practice. Early Alzheimer’s disease. N Engl J Med362: 2194–2201. PMID: 20558370
  • Ramachandran, TS and Ramachandran, A. 2020. Prion-related diseases. Medscape
  • Sheehan, B. 2012. Assessment scales in dementia. Ther Adv Neurol Disord5: 349–358. PMID: 23139705

About the author

Gary R. Simonds, MD MHCDS FAANS
Gary is a professor at Virginia Tech Carilion School of Neuroscience and Virginia Tech Carilion School of Medicine.
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