Progressive Multifocal leukoencephalopathy (PML)

PML continues be a nemesis for the antibody based therapies. The new CD30 antibody, Brentuximab, has been associated with PML.

http://www.ncbi.nlm.nih.gov/pubmed/22472351

Cerebellopontine Angle Masses

Vestibular schwannoma 75%
Meningioma 10%
Epidermoid 5%
Facial nerve schwannoma 4%
Aneurysm (vertebral,basilar,PICA)
Brain stem glioma
Arachnoid cyst
Paraganglioma
Hematogenous metastatis
Subarachnoid spread of tumors
Lipoma
Hemangioma
Choroid plexus papilloma
Ependymoma
Desmoplastic medulloblastoma


Ref :Yousem and Grossman Neuroradiology

Charles Bonnet Syndrome

A beautiful explanation of visual hallucination by Oliver Sacks at TED.

http://www.ted.com/talks/lang/en/oliver_sacks_what_hallucination_reveals_about_our_minds.html

Brain Dead

Brain dead patients can display impressive spinal reflex movements, including the dramatic "Lazarus sign" (bilateral arm flexion, shoulder adduction, raising the arms and crossing the hands). These are all ostensibly due to local spinal cord reflexes, which have become autonomous and are under no suprasegmental control. Similarly, triple flexion response in which extension of great toe is accompanied by dorsiflexion of the foot and flexion of the knee and the hip.


Bueri JA, Saposnik G, Maurino J, et al. Lazarus` sign in brain death. Mov Disord 2000;15:583-586

Prognostic groups in Epilepsy.

1. Excellent Prognosis : 20-30% ; genetic etiology such as Benign childhood epilepsy with centrotemporal spikes, benign myoclonic epilepsy of childhood, benign neonatal seizures.Often remission occurs without AED treatment.

2. Good Prognosis : 30-40% ; epilepsy is easily controlled with AEDs. Remission is often permanent after discontinuation of medications. eg. Childhood absence epilepsy, epilepsy with generalized tonic-clonic seizures on awakening, and some focal seizures.

3. Uncertain prognosis : 10-20% ; AEDs are suppressive rather than curative.In this group medications must be continued for seizure control. eg. Juvenile myoclonic epilepsy (JME) and most of focal seizures.

4. Bad Prognosis : 20%; Most treatment including surgery reduce the incidence of seizures only partially. eg. Infantile spasms, Lennox- Gastaut syndrome, Tuberous sclerosis.

Ref : Bradley 2008

Causes of Daytime Sleepiness

1. Medications (sedatives, tranquilizers, anticonvulsants,antihistaminics, anti depressants, Beta blockers,dopamine agonists, L-dopa, alcohol abuse)

2. Acute medical illness of mononucleosis type, including mundane respiratory and gastrointestinal infections

3. Post-surgical, post-concussive and post-anesthetic states

4. Chronic neurologic diseases- MS, Dementias

5. Depression

6. Metabolic derangements - hypothyroidism, Addison`s disease, severe diabetes

7. Encephalitic disease - Post Viral encephalitis, Trypanosomiasis, Encephalitis lethargica (historical)

8. Lesions of hypothalamus - Kleine - Levin syndrome, Hypothalamic tumor or granuloma

9. Sleep apnea syndrome : Central and Obstructive

10. Narcolepsy - cataplexy

11. Idiopathic hypersomnia

(From : Adams and Victor)

Phenytoin metabolism

As serum concentration of phenytoin rises, particularly above 15mg/l, the metabolism slows substantially. This is called 'zero order kinetics'. At levels below 15 mg/l, doubling the dose will lead to doubling of serum concentration and the half life is 24 hrs. As metabolism slows at higher concentrations, even a 50 mg change in dose can double the serum concentration, and the half life increases to 48-70 hrs.Since the half life is so prolonged, a steady state after dose adjustments may not occur for weeks, with serum levels slowly rising over this time. This can easily lead to serious phenytoin toxicity.

Ref : Therapeutic Strategies in Epilepsy ( French and Delanty)