Saturday, March 19, 2011

Internuclear ophthalmoplegia

In this video Daroff explains the INO completely. Do check it out, if only to see Daroff's completely 1960's OKN strip. We gotta get one of those for Paul Lee.

Bilateral Internuclear ophthalmoplegia

The disorder is caused by injury or dysfunction in the medial longitudinal fasciculus(MLF), a heavily-myelinated tract that allows conjugate eye movement by connecting the paramedian pontine reticular formation (PPRF) -abducens nucleuscomplex of contralateral side to the oculomotor nucleus of the ipsilateral side.

In young patients with bilateral INO, multiple sclerosis is often the cause. In older patients with one-sided lesions a stroke is a distinct possibility. Other causes are possible. (Wiki)

Friday, March 18, 2011

Doll's eye sign in comatose patient

This show the normal Doll's eyes response in a patient who has coma from bicortical dysfunction

Absent Doll's eyes in patient with massive brainstem dysfunction

Absent Doll's eye movements to VOR. Does not rule out absence to Cold calorics though.

Friday, March 11, 2011

MRI features of CSF Hypotension



Pretreatment (upper row) and post-treatment (lower row) axial fluid-attenuated inversion recovery magnetic resonance imaging (MRI) (A) showing resolution of bilateral subdural haematomas (arrowheads) and engorgement of the superior sagittal sinus (arrow) in a 35-year-old man; axial T1-weighted MRIs after intravenous administration of gadolinium (B) showing resolution of enhancement of the pachymeninges (arrowheads) in a 39-year-old woman; and sagittal T1-weighted MRIs showing resolution of sagging of the brain [flattening of the pons with obliteration of the prepontine cistern (arrowheads) and downward displacement of the cerebellar tonsils mimicking a Chiari malformation (arrowhead)] and hyperaemia/enlargement of the pituitary gland (arrow) in a 41-year-old woman. Also note restoration of ventricular size post treatment in all panels.

Schievink W Cephalalgia 2008;28:1345-1356

Tuesday, March 8, 2011

Hot Crossed Buns sign in Multisystem Atrophy-Cerebellar type

The hot cross bun appearance is seen in patients with MSA-c. The sign is due to a selective loss of myelinated transverse pontocerebellar fibers and neurons in the pontine raphe with preservation of the pontine tegmentum and corticospinal tracts (1). Other investigators (2) have demonstrated a similar pattern of neuronal loss in a patient with parkinsonism, the neuronal loss being secondary to presumed vasculitis, and proposed that the sign may reflect wallerian degeneration of transverse pontocere- bellar fibers secondary to vasculitic infarction. Regardless of the mechanism, this pattern of selective neuronal depletion results in a cross-shaped hyperintensity in the pons on T2-weighted MR images. Radiology: Volume 245: Number 2—November 2007

Marchiafava-Bignami disease

MARCHIAFAVA-Bignami disease (MBD) is the symmetrical demyelination of the middle portion of the corpus callosum that can be observed in people with chronic alcoholism. Its evolution may be fatal or lead to various degrees of slowly evolving cognitive impairment. Patients with a benign course have been reported. Scattered reports exisit that it may respond to thiamine injections and therefore may be a variant of Wernicke's encephalopathy.ARCHNEUROL/VOL56, JAN1999




Concentric ring of Balo

Balo's Concentric Sclerosis, is considered a rare variant of multiple sclerosis (MS), is characterized by a lesion consisting of rings of demyelination alternating with rings of intact myelin. Lesions have been observed in the spinal cord, cerebellum, brain stem, optic chiasm, and cerebral hemispheres.2 BCS is thought to be slightly more prevalent among males than among females, and to be particularly prevalent among younger men.3 Traditionally, BCS has been considered to be a rapidly fatal disease. With the advent of MRI, patients like the individual described in this Case Study have been diagnosed early, received treatment, and survived for months or years. These results imply that some cases of BCS might have a mild course, and cases that could have been effectively treated but previously remained unrecognized are now being discovered. A classification scheme for BCS has been proposed that defines the disease into the following three subtypes: a self-limited, monophasic illness; relapsing–remitting demyelination; and the classically described, primary rapidly progressive course. Nature Clinical Practice Neurology (2007) 3, 349-354


Wernicke's Encephalopathy

Basal ganglia and dentate nucleus damage in Carbon Monoxide poisoning


Caudate atrophy in Wilson's disease


Face of Panda sign in Wilson's disease

Brain MRI showed bilateral T2 hyperintensity involving putamen, thalami, and brainstem. The midbrain “panda sign” is due to high signal in the tegmentum, normal signals in the red nuclei and lateral portion of the pars reticulata of the substantia nigra, and hypointensity of the superior colliculus.

Dina A. Jacobs, Clyde E. Markowitz, David S. Liebeskind, et al. Neurology 2003;61;969

Scattered vs String of pearls signs in MCA/ICA stenosis

Humming bird sign of PSP