Urgent considerations

See Differentials for more details

Any disease process that affects the central nervous system may present with memory loss and cognitive changes. In some cases these symptoms may be a harbinger of life-threatening disease and, therefore, should be treated promptly to avoid death or permanent disabilities.

Acute memory loss

Stroke

Consider ischaemic or haemorrhagic stroke in cases of acute memory loss (occurring over minutes to hours). An acute stroke should be ruled out by a detailed history and physical examination, as well as appropriate imaging. Special attention should be paid to the posterior circulation, which supplies most of the limbic structures, including the hippocampus. Furthermore, bilateral thalamic strokes can also cause acute memory loss or other cognitive dysfunction.[25][26] Symptoms of limb and/or facial weakness, paraesthesia, numbness, and speech difficulty may occur in anterior circulation stroke. Visual loss or double vision, dizziness, vertigo, and nausea can occur in posterior circulation strokes.

In most cases, an urgent computed tomography (CT) head without contrast is appropriate and readily accessible. This can detect acute intracranial haemorrhage and large infarcts, and permits the clinician to assess the patient’s suitability for thrombolysis.[27][28] If the patient has had stroke symptoms for fewer than 6 hours, non-contrast CT is often performed first. If the patient has had stroke symptoms for longer than 6 hours, magnetic resonance imaging (MRI) is recommended as the initial investigation. MRI can be performed without contrast for patients with renal failure or contrast allergy.[29]

Seizures

Emergency management involves securing the airway and terminating the seizure. Assess the patient using an ‘ABCDE’ approach to airway, breathing, circulation, disability, and exposure. If the airway is clear, most patients breathe effectively during a seizure. Administer supplemental oxygen. Check blood glucose in all patients with a suspected seizure. Hypo- and hyperglycaemia may cause seizures and should be corrected if present.[30]

Electroencephalogram is essential to rule out sub-clinical seizures when seizures are suggested by the clinical presentation. In such cases, patients might have other symptoms in addition to memory loss, such as staring spells, sudden halting of speech, or subtle facial, lip, or eye twitching. For more acute declines in mental status without other explanation, non-convulsive status epilepticus should be considered, in which there are no motor manifestations of seizures.[31] Initiate immediate treatment with anticonvulsants if the diagnosis is confirmed.

Subacute memory loss

For subacute memory loss (i.e., over days to weeks), the possibility of infections, toxic-metabolic disorders, mass lesions, and inflammatory processes should be considered.

Infections

Herpes simplex virus (HSV) can cause isolated memory loss through an infectious limbic encephalitis. Once HSV encephalopathy is suspected, treatment with intravenous aciclovir should be initiated immediately.

Inflammation

Limbic encephalitis might be caused by an autoimmune process as well, such as antibody-mediated limbic encephalitis often secondary to paraneoplastic or non-paraneoplastic antibodies. If paraneoplastic in origin, the underlying cancer should be treated. Limbic encephalitis, whether paraneoplastic or non-paraneoplastic, is typically treated with corticosteroids, plasmapheresis, and/or intravenous immunoglobulin (IVIG).

Hashimoto's encephalopathy generally responds well to high-dose corticosteroids or immunosuppressants. IVIG or plasmapheresis might also be used.[32][33][34][35][36][37]

Wernicke-Korsakoff's syndrome

Wernicke-Korsakoff's syndrome results from thiamine deficiency and may present in patients at risk for nutritional deficiencies (or metabolic disorders). The diagnosis should be considered in any patient with at least two of the following:[23]​​

  • nutritional deficiency

  • altered mental state or memory impairment

  • oculomotor abnormalities (e.g., nystagmus, ophthalmoplegia)

  • cerebellar dysfunction (e.g., gait disturbance, ataxia).

Urgent treatment is essential to minimise memory loss. Treatment is intravenous thiamine. The administration of glucose can worsen the disease process and, therefore, thiamine should always be administered simultaneously in emergency situations. Memory loss (encoding deficits) might be permanent or improve to a limited extent.[38]

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