Seizure in infantile spasms

Do you see the abnormality?  Surprisingly in this case it's not on the left side!  The high voltage chaos that looks as good right-side-up as up-side-down is characteristic for hypsarrhythmia in infantile spasms.  However, what should catch your eye is the pseudonormalization on the right half of the record: this is a seizure in infantile spasms – high frequency, low amplitude.  Neither side is normal, but that relative depression of the record with a global high frequency oscillation doesn't look normal for the record in this presumably awake child.

Absense seizure

What's going on?  According to Dr. Kaplan, one of 4 things: normal EEG activity, focal abnormality, global abnormality, seizure.  In this case, even if you didn't recognize the ~3Hz spike-wave complexes characteristic of an absense seizure, you could still figure out where you are by comparing side-to-side (odd numbers on the left; even numbers on the right) to know it's a global process of rhythmic activity (everything is firing together at about 3 cycles per second) that is high voltage (notice the scale in the bottom right corner showing our vertical scale at 300mV; normal is 70-100mV).  This is one of the reasons we do hyperventilation during our EEGs.

CO poisoning

This is a diffusion-weighted image (DWI).  Notice the demonstration of the globus pallidus diffusion restriction, but also DWI changes due to toxic insult...the splenium of the corpus callosum is ravaged, as is the subcortical white matter.  The deep gray matter and the splenium of the corpus callosum are highly sensitive to hypoxic/anoxic insult (as are the cortex and cerebellum).

Correlate the MRI to the classic pathologic findings in the first few hours after carbon monoxide poisoning: the brain is swollen, congested and cherry-red. After 24-48 hours of survival, scattered petechial hemorrhages may be seen in white matter with larger hemorrhages in the pallidum (arrows).

ADEM

In clinically defined cases of ADEM, the MRI will often demonstrate multifocal areas of increased T2-weighted (T2W) signal abnormalities in the CNS white matter, with or without gray matter involvement. Some authors have proposed that ADEM lesions are indistinct and lack sharply defined borders ("fluffy and diffuse") characteristic of MS lesions.  Although ADEM lesions (of similar age) should all hypothetically enhance with gadolinium, this finding is rarely seen, and gadolinium enhancement may even be absent.

Early MRI series identified overlap in lesion location and distribution between ADEM and MS, but also highlighted features of ADEM that are unusual in MS, such as symmetric bilateral disease, relative sparing of the periventricular white matter, or deep gray matter involvement.64 Absolute and relative periventricular sparing on MRI is typical of ADEM, and was present in 78% of patients with ADEM. However, 22% of ADEM patients had a periventricular lesion pattern indistinguishable from that seen in MS, and the characteristic corpus callosum long axis lesions (Dawson’s fingers), together with the finding of only well-defined lesions, were completely specific indicators of relapse/progression to MS.

Susac's syndrome

Susac syndrome (SS) consists of the triad of encephalopathy, branch retinal artery occlusions (BRAO), and hearing loss. The encephalopathy manifests with headache, confusion, memory loss, behavioral changes, dysarthria, and occasional mutism. The BRAO may be extensive or subtle; if the posterior pole of the retina is involved, patients may complain
of impaired vision. These BRAO are usually bilateral and may be the presenting features of the illness, or occur later in the clinical The MR scans in SS show a rather distinctive pattern of supratentorial white matter lesions that always involve the corpus callosum. There is often deep gray matter, posterior fossa involvement, and frequent parenchymal with occasional leptomeningeal enhancement. The central callosal lesions in Susac’s differ from multiple sclerosis as the ependymal undersurface of the corpus callosum is usually involved and callosal atrophy is usually seen in demyelinating disaese. Central involvement and an appropriate clinical picture should support the diagnosis of SS in patients with at least two of the three features of the clinical triad. NEUROLOGY 2003;61:1783–1787

See Abid's Susac DWI for another nice view

CADASIL MRI

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited, autosomal dominant condition caused by mutations of the Notch3 gene. Affected individuals have migraine, mood disturbance, and recurrent strokes, often progressing to subcortical dementia and premature death. MRI findings include focal lacunar infarcts and diffuse T2-weighted hyperintensity, or leukoaraiosis. Temporal pole hyperintensity is a radiologic marker of CADASIL. Involvement of the external capsule and corpus callosum are also characteristic findings that may help to distinguish the disease. Neurology March 13, 2001 vol. 56 no. 5 628-634

Status epilepticus MRI findings

Hotter than a cup of coffee! Note: DWI imaging increased signal in thalamus, insula and cortex. Note profound hippocampal involvement on axial FLAIR and DWI images. On FLAIR images there is significant hippocampal and temporal lobe involvement. No cells on LP. EEG shows ongoing right temporal seizures. We think she was having three seizures without loss of consciousness or convulsions every 20 minutes for a week before this scan



DWI with temporal lobe involvement

DWI with insula and thalamic involvement

FLAIR showing significant hippocampal and temporal love involvement. All this injury is felt secondary to the ongoing uncontrolled seizure activity.