Table 1.
Summary of common disease processes causing bilateral temporal lobe disease
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 |
*HHV-6 – Human Herpes Virus -6
†OTC - Ornithine TransCarbamylase
‡CADASIL - Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy