Skip to main content
. 2016 Feb 24;7(2):265–274. doi: 10.1007/s13244-016-0481-x

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