Proposed criteria for Refractory Migraine

A) Primary diagnosis ICHD II Migraine or Chronic Migraine
B) Significant interference with QOL despite
• modification of triggers, lifestyle factors
• adequate trials of acute and preventive medicines

Preventive medicines (at least 3 of 4)
1 Beta Blocker
2 Anticonvulsant
3 Tricyclics
4 Calcium channel blocker

Abortive medicines (all)
1 Both a triptan and DHE intranasal or injectable
2 Either a non steroidal anti-inflammatory drug or combination analgesics

Adequate trial  - 2 months/ less if stopped because of adverse effects, with dose being optimal/ maximum tolerated

Modifiers +/-
1 With or without medication overuse
2 With or without significant disability (MIDAS score >11)

Criteria for refractory migraine (proposed)

Revised Criteria Alzheimer's (Du Bois)

Probable AD: A plus one or more supportive features B, C, D, or E

Core diagnostic criteria

A. Presence of an early and significant episodic memory impairment that includes the following features:

1. Gradual and progressive change in memory function reported by patients or informants over more than 6 months

2. Objective evidence of significantly impaired episodic memory on testing: this generally consists of recall deficit that does not improve significantly or does not normalise with cueing or recognition testing and after effective encoding of information has been previously controlled.

The episodic memory impairment can be isolated or associated with other cognitive changes at the onset of AD or as AD advances

Supportive features

B. Presence of medial temporal lobe atrophy

•  Volume loss of hippocampi, entorhinal cortex, amygdala evidenced on MRI with qualitative ratings using visual scoring (referenced to well characterised population with age norms) or quantitative volumetry of regions of interest (referenced to well characterised population with age norms)

C. Abnormal cerebrospinal fluid biomarker

• Low amyloid β1–42 concentrations, increased total tau concentrations, or increased phospho-tau concentrations, or combinations of the three

• Other well validated markers to be discovered in the future

D. Specific pattern on functional neuroimaging with PET

• Reduced glucose metabolism in bilateral temporal parietal regions

• Other well validated ligands, including those that foreseeably will emerge such as Pittsburg compound B or FDDNP

E. Proven AD autosomal dominant mutation within the immediate family

Exclusion criteria

History

• Sudden onset 

• Early occurrence of the following symptoms: gait disturbances, seizures, behavioural changes

Clinical features

• Focal neurological features including hemiparesis, sensory loss, visual field deficits

• Early extrapyramidal signs

Other medical disorders severe enough to account for memory and related symptoms

• Non-AD dementia 

• Major depression 

• Cerebrovascular disease 

• Toxic and metabolic abnormalities, all of which may require specific investigations 

• MRI FLAIR or T2 signal abnormalities in the medial temporal lobe that are consistent with infectious or vascular insults

Criteria for definite AD

AD is considered definite if the following are present:

• Both clinical and histopathological (brain biopsy or autopsy) evidence of the disease, as required by the NIA-Reagan criteria for the post-mortem diagnosis of AD; criteria must both be present

• Both clinical and genetic evidence (mutation on chromosome 1, 14, or 21) of AD; criteria must both be present

Criteria for Sjogren's syndrome

I. Ocular Symptoms (at least one)

Dry eyes >3 months?
Foreign body sensation in the eyes?
Use of artificial tears >3x per day?

II. Oral Symptoms (at least one)

Dry mouth >3 months?
Recurrent or persistently swollen salivary glands?
Need liquids to swallow dry foods?

III. Ocular Signs (at least one)

Schirmer's test, (without anesthesia) ≤5 mm/5 minutes
Positive vital dye staining (van Bijsterveld ≥4)

IV. Histopathology 

Lip biopsy showing focal lymphocytic sialoadenitis
(focus score ≥1 per 4 mm2)

V. Oral Signs (at least one)

Unstimulated whole salivary flow (≤1.5 mL in 15 minutes)
Abnormal parotid sialography3
Abnormal salivary scintigraphy4

VI. Autoantibodies (at least one)

Anti-SSA (Ro) or Anti-SSB (La)

For a primary Sjögren’s diagnosis:
a. Any 4 of the 6 criteria, must include either item IV (Histopathology) or VI (Autoantibodies)
b. Any 3 of the 4 objective criteria (III, IV, V, VI)

For a secondary Sjögren’s diagnosis:
In patients with another well-defined major connective tissue disease, the presence of one symptom (I or II) plus 2 of the 3 objective criteria (III, IV and V) is indicative of secondary SS.

Exclusion Criteria

Past head and neck radiation treatment
Hepatitis C infection
Acquired immunodeficiency syndrome (AIDS)
Pre-existing lymphoma
Sarcoidosis
Graft versus host disease
Current use of anticholinergic drugs

My present stand on DBS in India

If I receive a mail enquiry from someone I do not know, I give them a list of places where DBS is done. If someone I know asks, I tell them pros and cons and give a list mentioning where the largest numbers are from. I specifically mention the purely symptomatic nature of therapy, the requirement for intensive follow up and the problems of DBS/ dopaminergic dose reduction on cognition and behavior. However if it is a relative who asks, I would not recommend DBS if they have to sell land or leave their job and relocate. I tell them that optimal medical and physical therapy is still very much an option; that most available literature recommending DBS is of short duration (6 to 24 months) or inadequate numbers if longer duration, implying that the long term benefits are being extrapolated. (I don't mention conflict of interest due to involvement of the company manufacturing the device.)

Electrical injury and non progressive motor syndromes

J Neurol Neurosurg Psychiatry. 2007 May;78(5):450-3. Epub 2006 Nov 10.

Electrical injury and amyotrophic lateral sclerosis: a systematic review of the literature.

Abhinav K, Al-Chalabi A, Hortobagyi T, Leigh PN.

Queen Elizabeth Hospital, London, UK.

Electrical injury may act as a potential precipitating or risk factor for amyotrophic lateral sclerosis (ALS). A systematic review of the literature was undertaken to assess the relationship between electrical injury and the development of ALS. Information for the review was obtained using five medical databases, and from manual searching of individual papers. Patients presenting with a neurological syndrome after electrical injury, including lightning, were included and classified into four categories: ALS; progressive upper motor neurone (UMN) syndrome; progressive lower motor neurone (LMN) syndrome; and non-progressive syndrome. Linear regression and chi2 testing were used for analysis of the data. 96 individuals, comprising 44 with ALS, 1 with a progressive UMN syndrome, 7 with a progressive LMN syndrome and 44 with a non-progressive syndrome, were identified from 31 papers with publication dates between 1906 and 2002. The median interval between electrical injury and disease onset was 2.25 years for all progressive syndromes and just over 1 week for the non-progressive syndrome. The more severe the shock (excluding lightning), the

more likely individuals were to have a non-progressive motor syndrome. A non-progressive spinal cord syndrome is associated with more severe electrical injury. Overall, the evidence reviewed does not support a causal relationship between ALS and electric shock.

PMCID: PMC2117843

PMID: 17098839 

The flushing patient

http://site2012.View blogsbd-sp.org.br/public/img/destaques/destaque06.pdf

Neurology and Psychiatry

C Butler, A Z J Zeman. Neurological syndromes which can be mistaken for psychiatric conditions. J Neurol Neurosurg Psychiatry 2005;76:i31-i38.

All illness has both psychological and physical dimensions. This may seem a startling claim, but on reflection it is uncontroversial. Diseases don’t come to doctors, patients do—and the processes by which patients detect, describe, and ponder their symptoms are all eminently psychological. This theoretical point has practical implications. If we adopt a “bio-psycho-social” approach to illness generally, one which recognises the biological, psychological, and social aspects of our lives, we become less likely to neglect the treatable psychological origins of many physical complaints (from globus hystericus to full blown conversion disorder) and the treatable psychological consequences (such as depression and anxiety) of much physical disease.