Increased Blink Rate Causes

Eye blinking symptoms include both an increased and decreased rate of blinking. 

Most commonly, increased eye blinking results from eye irritation caused by bright light, dust, smoke, or a foreign body in the eye. Allergies, infections, and dry eye may also increase the rate of blinking. Conditions of stress, anxiety or fatigue may lead to increased blinking. 

Facial tics, which are habitual repetitive twitches or movements of the face that occur most often in children, may include increased blinking. Congenital glaucoma is a rare cause of increased blinking.

Eye blinking symptoms may also be caused by conditions occurring in the nervous system. Blepharospasm, a condition characterized by rapid, uncontrolled blinking and even involuntary eye closure, is classified as a dystonia, in which the nervous system signals the muscles to contract inappropriately. These spasms may be accompanied by other quick facial changes such as eye rolling or grimacing. Increased blinking may also occur in several nervous system disorders, such as stroke, tardive (slow or belated onset) dyskinesia, Tourette’s syndrome, or Aicardi syndrome (rare organic brain disorder acquired in early childhood).

Conditions which cause decreased blinking.

Few conditions which cause decreased blinking. 
Parkinson's disease, 
Graves disease or thyroid opthalmopathy
Chronic cannabis/cocaine use
Computer Vision Syndrome
Normal Aging

G B Syndrome mimics

False-positive AChR-ab tests

False-positive AChR-ab tests are rare, but reported in

autoimmune liver disease,
systemic lupus,
inflammatory neuropathies,
amyotrophic lateral sclerosis,
penicillamine-treated patients with rheumatoid arthritis,
patients with thymoma but without MG, and
first-degree relatives of patients with acquired autoimmune MG.

Other Causes of Positive EdrophoniumTest

Improvement after edrophonium is not unique to MG, and also seen in
congenital myasthenic syndromes (CMS),
the Lambert–Eaton syndrome (LES),
intracranial aneurysms,
brainstem lesions,
cavernous sinus tumors,
end-stage renal disease, and
muscle diseases affecting the ocular muscles

GBS vs Critical Illness Neuropathy

• GBS and CIP are important causes of weakness in ICU and distinguishing between them is important due to the management and prognostic implications

COMPARISON

	GBS	CIP
History	Recent GI or resp illness. Progressive bilateral symmetric paralysis. Subtypes can be more localized e.g. MF opthalmoplegia and ataxia. Sensory involvement is common. Areflexic. Autonomic involvement may be present	Always occurs in association  with a critical illness in particular severe sepsis. May have an association with encephalopathy in early stages. It is a symmetrical weakness. May have muscle tenderness, hyporeflexic, diminished distal sensation Not associated with autonomic involvement
Examination	Albuminocytologic dissociation in CSF. Identification of infection with campylobacter, mycoplasma, EBV,Varicella, CMV. Elevated csf IGG levels and possible serum antiganglioside antibodies	Elevated CK which may be transient.
Investigations	When demyelinating form is present, you get a reduction in conduction velocity as well as reduction in CMAP In axonal forms however it is  only the distribution of the findings that helps determine the diagnosis	A axonal neuropathy resulting in a decreased CMAP without a reduction in conduction velocity

Stages of Myasthenia Gravis

Symptoms fluctuated over a relatively short period of time and then became progressively severe for several years (active stage). 

The active stage is followed by an inactive state in which fluctuations in strength still occurred but are attributable to fatigue, intercurrent illness, or other identifiable factors. 

After 15 to 20 years, weakness often becomes fixed and the most severely involved muscles are frequently atrophic (burnt-out stage).

Geniculocalcarine fibers, Meyer's fibers and vision conduction

Visual Field defects

Tics- Simple and Complex

A tic is a brief, repetitive, purposeless, nonrhythmic, involuntary movement or sound. Tics that produce movement are called “motor tics,” while tics that produce sound are called “vocal tics” or “phonic tics.” Motor tics seems to be more common than vocal tics.

Tics are often characterized by whether they are “simple” or “complex.” A simple tic involves one muscle group or one simple sound. Many simple motor tics are associated with the face/head/neck region, such as eye blinking, head jerking, shoulder shrugging, mouth grimacing, etc. Simple vocal tics include throat-clearing sounds, grunting, sniffing, and coughing. Simple motor tics of the face and head/neck region are the most common first tics in children.

A complex tic involves a coordinated movement produced by a number of muscle groups (complex motor tic) or a linguistically meaningful utterance or phrase (complex vocal tic). As examples, complex motor tics can involve touching objects or other people, jumping up and down, spinning around, or even more complex motor sequences such as imitating someone else’s actions (echopraxia) or exhibiting inappropriate or taboo gestures or behaviors (copropraxia). Complex vocal tics may involve having to repeat one phrase over and over, whether it is something one heard (echolalia) or one’s own last words (palilalia).

List of Pseudodystonia

Classification of Dystonia

Cortical Venous System

Cervicogenic Headache

Cervicogenic Headache

A. Pain localised to the neck and occipital region. May project to forehead, orbital region, temples, vertex or ears

B. Pain is precipitated or aggravated by special neck movements or sustained postures

C . At least one of the following:

1. Resistance to or limitation of passive neck movements

2. Changes in neck muscle contour, texture, tone or response to active and passive stretching and contraction

3. Abnormal tenderness of neck muscles

D. Radiological examination reveals at least one of the following

1. Movement abnormalities in flexion/extension

2. Abnormal posture

3. Fractures, congenital abnormalities, bone tumours, rheumatoid arthritis or other distinct pathology (not spondylosis or osteochondrosis)

Tension-Type Headache

Tension-Type Headache

A. Headache lasting from 30 minutes to seven days

B. At least two of the following criteria:

1. Pressing/tightening (non-pulsatile) quality

2. Mild or moderate intensity (may inhibit, but does not prohibit activity

3. Bilateral location

4. No aggravation by walking, stairs or similar routine physical activity

C . Both of the following:

1. No nausea or vomiting (anorexia may occur)

2. Photophobia and phonophobia are absent, or one but not both are present

Cluster Headache

Cluster Headache

A. At least five attacks of severe unilateral orbital, supraorbital and/or temporal pain lasting 15 to 180 minutes untreated, with one or more of the following signs occurring on the same side as the pain

1. Conjunctival injection

2. Lacrimation

3. Nasal congestion

4. Rhinorrhoea

5. Forehead and facial sweating

6. Miosis

7. Ptosis

8. Eyelid oedema

B . Frequency of attacks from one every other day to eight per day

Migraine Criteria- With Aura and Without Aura

Migraine without aura (MO) diagnostic criteria

A. At least five headache attacks lasting 4 - 72 hours (untreated or unsuccessfully treated), which has at least two of the four following characteristics:

1. Unilateral location

2. Pulsating quality

3. Moderate or severe intensity (inhibits or prohibits daily activities)

4. Aggravated by walking stairs or similar routine physical activity

B. During headache at least one of the two following symptoms occur:

1. Phonophobia and photophobia

2. Nausea and/or vomiting

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Migraine with aura (MA) diagnostic criteria

A. At least two attacks fulfilling with at least three of the following:

1. One or more fully reversible aura symptoms indicating focal cerebral cortical and/or brain stem functions

2. At least one aura symptom develops gradually over more than four minutes, or two or more symptoms occur in succession

3. No aura symptom lasts more than 60 minutes; if more than one aura symptom is present, accepted duration is proportionally increased

4. Headache follows aura with free interval of at least 60 minutes (it may also simultaneously begin with the aura

B. At least one of the following aura features establishes a diagnosis of migraine with typical aura:

1. Homonymous visual disturbance

2. Unilateral paresthesias and/or numbness

3. Unilateral weakness

4. Aphasia or unclassifiable speech difficulty

Demyelination vs Dysmyelination

Demyelination is a term used to describe the destruction of a substance called myelin that surrounds axonal fibres. This is caused by diseases that damage the myelin sheath or the cells that form it.

One of most common forms of autoimmune demyelinating disease is MS.Other autoimmune disorders that can cause demyelination include transverse myelitis, acute disseminated encephalomyelitis, Guillain-Barré Syndrome, chronic inflammatory demyelinating polyneuropathy, central pontine myelinosis, Charcot Marie Tooth disease and leukodystrophy.

Dysmyelination on the other hand, is a term used to describe the defective structure and function of myelin sheaths. Unlike demyelination, nerve lesions are not a feature of dysmyelination.

Dysmyelination disorders often arise from hereditary mutations that affect the synthesis and formation of myelin. The disorders can be categorized into those that affect mainly the white brain matter and those that affect both the white and grey matter. Dysmyelination disorders are also referred to as leukodystrophies and the most common example is metachromatic leukodystrophy.

Hallervorden-Spatz Disease

Presentation

History

Symptoms in Hallervorden-Spatz disease (HSD) include the following:

• Dystonia - A prominent and early feature
• Significant speech disturbances - Can occur early
• Dysphagia - A common symptom; caused by rigidity and corticobulbar involvement
• Dementia - Present in most individuals with HSD
• Visual impairment - Caused by optic atrophy or retinal degeneration; not uncommon and can be the presenting symptom of the disease, although this is rare
• Seizures - Have been described [18]

Clinical manifestations of HSD vary from patient to patient. The symptoms usually begin in the first decade with a motor disorder of extrapyramidal type and gait difficulty. Extrapyramidal symptoms dominate the clinical picture and include rigidity, slowness of movement, dystonia, choreoathetosis, and tremor.

In some patients, extrapyramidal dysfunction may be delayed for several years, and spasticity and dysarthria may be the presenting symptoms.

Physical Examination

Physical examination reveals signs consistent with extrapyramidal and corticospinal dysfunction. In addition to rigidity, dystonia, and chorea, patients may exhibit spasticity, brisk reflexes, and extensor plantar responses.

Based on the common clinical features, the following diagnostic criteria for HSD have been proposed.[18] For a definitive diagnosis, all of the obligate findings and at least 2 of the corroborative findings should be present. None of the exclusionary factors should be present.

Obligate features of HSD include the following:

• Onset during the first 2 decades of life
• Progression of signs and symptoms
• Evidence of extrapyramidal dysfunction, including 1 or more of the following: dystonia, rigidity, choreoathetosis

Corroborative features include the following:

• Corticospinal tract involvement
• Progressive intellectual impairment
• Retinitis pigmentosa and/or optic atrophy
• Seizures
• Positive family history consistent with autosomal recessive inheritance
• Hypointense areas on magnetic resonance imaging (MRI) involving the basal ganglia
• Abnormal cytosomes in circulating lymphocytes and/or sea-blue histiocytes in bone marrow

Exclusionary features include the following:

• Abnormal ceruloplasmin levels and/or abnormalities in copper metabolism
• Presence of overt neuronal ceroid lipofuscinosis, as demonstrated by severe visual impairment and/or seizures that are difficult to control
• Predominant epileptic symptoms
• Severe retinal degeneration or visual impairment preceding other symptoms
• Presence of familial history of Huntington chorea and/or other autosomal, dominantly inherited neuromovement disorders
• Presence of caudate atrophy on imaging studies
• Deficiency of hexosaminidase A
• Deficiency of ganglioside monosialic acid-1 (GM1)–galactosidase
• Nonprogressive course
• Absence of extrapyramidal signs