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Table 1 Summary of common disease processes causing bilateral temporal lobe disease

From: Bilateral temporal lobe disease: looking beyond herpes encephalitis

Disease

Main clinical characteristics

Main imaging characteristics

Main differential diagnosis

Herpes encephalitis

Fever, headaches, seizures and altered mental status

Asymmetric bilateral temporal lobe disease; insular disease; stops at the lateral putaminal border. Gyral enhancement and cortical microbleeds on MRI

HHV-6 encephalopathy, fungal infection, adult type OTC deficiency, glioma

HHV-6* encephalop athy

Change in mental status, loss of short-term memory and seizures about 3 weeks post-transplant

Symmetric mesial temporal lobe and limbic system disease

Herpes encephalitis, limbic encephalitis

Fungal infection

Spread of paranasal sinus infection in immune-compromised patients

Brain edema, hemorrhages, irregular enhancement. Paranasal sinus infection

Herpes encephalitis

Limbic encephalitis

Subacute presentation with personality changes, irritability, depression, dementia, seizures and short-term memory loss

Unilateral or bilateral mesio-temporal disease. Enhancement may occur as well as involvement of additional limbic system components and other brain regions

HHV-6 encephalopathy, Alzheimer disease, Fronto-temporal dementia

Alzheimer disease

Cognitive decline interfering with daily activities

Disproportional asymmetric volume loss in the mesial temporal structures

Fronto-temporal dementia, limbic encephalitis, remote insult (sequel of herpes encephalitis, trauma)

Fronto-temporal dementia

Changes in personality and behavior and decline in semantic performance

Asymmetric temporal lobe atrophy in semantic variant of the disease

Alzheimer disease, remote insult (sequel of herpes encephalitis, trauma)

Adult type OTC deficiency

Acute encephalopathy

Symmetric disease of the insula and cingulate gyrus with increased T2 signal and diffusion restriction, and without enhancement

Herpes encephalitis, glioma

Mesial temporal sclerosis

Complex partial seizures

Hippocampal atrophy and increased T2/FLAIR. Bilateral in 10 %

Limbic encephalitis, other temporal lobe epileptogenic diseases

Glioma

Insidious course of worsening neurological deficits; new onset seizures; change in mental status

Edema, infiltration and possible enhancement (depending on tumoral grade); possible spread along nerve tracts

Herpes encephalitis, limbic encephalitis, adult type OTC deficiency

Posterior circulation ischemia

Acute visual and memory deficits and altered mental status

Ischemic lesions in PCA territory

Herpes encephalitis

CADASIL

Recurrent strokes, migraine, cognitive decline

Focal lesions of increased T2 signal in anterior temporal lobe and external capsule. Periventricular and deep white matter lesions throughout the brain; lacunar infarctions

Microangiopathy, cerebral vasculitis

Trauma

History of traumatic insult

Anterior temporal cortical contusions and or epidural or subdural hematomas

Post-traumatic encephalomalacia may simulate atrophy

Radiation necrosis

History of prior radiation to the head and neck

Edema and enhancement within the radiation port

Herpes encephalitis, glioma

  1. *HHV-6 – Human Herpes Virus -6
  2. OTC - Ornithine TransCarbamylase
  3. CADASIL - Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy