Internal Capsule

Modified Ashworth Scale

Trophic changes

On a surface level, trophic changes are simply changes in soft tissue (skin, fascia, muscle), resulting from interruption of nerve supply (Baluk 1992). Neurogenic inflammation is continuing inflammation in the musculoskeletal system, generated by nerve impulses and the release of inflammatory substances from the sensory axon at the site of the original injury. These substances are typically, but not limited to: Substance P (SP), Calcitonic Gene Related Peptide (CGRP), and Neurokinin-A (NKA). Prolonged inflammation and pain can lead to protective muscle spasms, but it more commonly leads to an accumulation of fibrous tissue—which are trophic changes . Devor (1999) stated that the fibrous tissue forms trophic changes, which become palpable taut muscle bands and trigger points; such muscle dysfunction and spasm lead to compression of blood vessels, and decreased blood flow, implicating pain stimulation, and decreased joint mobility. The somatic motor system and the autonomic nervous system influence the skeletal muscular system by stimulating muscles to contract and nerves to secrete during the regulation of molecular organization of other cells, like collagen in soft tissue repair during rehabilitation of an injury. These effects are referred to as trophic, or nutritional, functions of the nervous system (Portenoy, 1994). The key to clinical treatment is to reverse the stimuli that trigger the noxious chemical and mechanical stimuli, which trigger the neurogenic inflammatory response. Manipulation of joints, manual muscle treatments, and interventions that directly target the nervous system like acupuncture and electro-stimulation are key allies in the minimization of trophic changes and the acceleration of soft tissue healing (Lombardi, 2012).

Basal Ganglia Anatomy

SCA

Investigations and DD of hypokalemic periodic paralysis

Salt Challange test

Oral Salt Loading Test

IV Salt Loading Test

Drugs to be Avoided that affect Renin & Aldosterone

Paper Grip test

White Hand sign

White Hand sign

The white hand sign is a medical sign observed as a visible whitening of skin on the hand when the subject elevates the hands above the shoulder girdle with fingers pointing to the ceiling and palms facing forward. The appearance of the paleness, sometimes cadaveric, in one or both hands is called the White Hand Sign. It results from this change in position causing a compression of the subclavian artery and temporary loss of circulation, as often occurs in patients with thoracic outlet syndrome, a complex syndrome involving the compression of various nerves and blood vessels between the axilla (armpit) and the base of the neck.

The use in the physical examination of a triad consisting of tenderness of the supraclavicular area, paleness and/or paresthesias on elevation of the hands, and weakness of the abductors and adductors of the 5th finger, will make the diagnosis of Thoracic Outlet Syndrome consistent and reproducible.

A new physical sign called the White Hand Sign is described. When used with the diagnostic triad in the routine physical examination, it will standardize the diagnosis of Thoracic Outlet Syndrome.

The White Hand Sign will objectively assess the postural vascular compression at the thoracic outlet. The absence of the color changes on the elevation of the hands should not be construed that Thoracic Outlet Syndrome is not present, severe nerve compression can exist without vascular compression.

Fornix

Parts of Sylvian Fissure

Degenerative Causes of Supranuclear Vertical Gaze Disorder

Degenerative Causes of Supranuclear Vertical Gaze Disorder

Progressive Supranuclear Palsy
Corticobasal ganglionic degenration
Parkinsons disease
Lewy Body disease
Whipple disease

Basal Ganglia

Daroff's Rules for CN 3

Keith Wagener Barker classification of Hypertensive Retinopathy

Modified Frisen Scale for Papilledema

CSFcirculation

Midbrain section

Cheiralgia Paresthetica - Handcuff Neuropathy- Wartenberg syndrome- wristwatch neuropathy

This neuropathy was first identified by Robert Wartenberg in a 1932 paper. Demographics- male:female ratio is 1:4, more common in women, age bracket is 20-70 years. 

Cheiralgia paraesthetica is a neuropathy of the hand generally caused by compression or trauma to the superficial branch of the radial nerve. The exact etiology is unknown, as it is unclear whether direct pressure by the constricting item is alone responsible, or whether edema associated with the constriction also contributes. Diagnostically it is often subsumed into compression neuropathy of the radial nerve as a whole (e.g. ICD-9 354.3), but studies and papers continue to use the older term to distinguish it from more extensive neuropathies originating in the forearm.

The most common cause is thought to be constriction of the wrist, as with a bracelet, wrist band, plaster cast or watchband (hence reference to "wristwatch neuropathy"). The patient may have history of trauma causing forearm fracture. It is especially associated with the use of handcuffs and is therefore commonly referred to as handcuff neuropathy. Other injuries or surgery in the wrist area can also lead to symptoms, including surgery for other syndromes such as de Quervain's.

The area affected is typically on the back or side of the hand at the base of the thumb, near the anatomical snuffbox, but may extend up the back of the thumb and index finger and across the back of the hand. 

The superficial sensory branch of the radial nerve arises from the bifurcation of the radial nerve in the proximal forear and travels deep to the brachioradialis in the forearm, emerging from between brachioradialis and ECRL 9cm proximal to radial styloid and bifurcates proximal to the wrist. The dorsal branch lies 1-3cm radial to Lister's tubercle and supplies 1st and 2nd web space. The palmar branch passes within 2cm of 1st dorsal compartment, directly over EPL and supplies dorsolateral thumb

Pathoanatomy- SRN compressed by scissoring action of  brachioradialis and ECRL tendons during forearm pronation, also by fascial bands at its exit site in the subcutaneous plane.

Symptoms include numbness, tingling, burning or pain (over dorsoradial hand). Symptom aggarvation is by motions involving repetitive wrist flexion and ulnar deviation. Since the nerve branch is sensory there is no motor impairment. 

Physical exam (provocative tests)-

Tinel's sign over the superficial sensory radial nerve (most common exam finding).

Finkelstein test increases symptoms in 96% of patients because of traction on the nerve

Investigations- X ray and NCV are of limited role.

Differential Diagnosis

It may be distinguished from de Quervain syndrome because it is not dependent on motion of the hand or fingers.

Lateral antebrachial cutaneous nerve (LACN) neuritis- positive Tinel's sign over LACN can be mistaken for positive Tinel's over superficial sensory radial nerve.

Intersection syndrome- may have dorsoradial forearm swelling, symptom exacerbation and "wet leather" crepitus on repeated wrist flexion/extension.

Symptoms commonly resolve on their own within several months when the constriction is removed- A superficial sensory cutaneous twig of the radial nerve is the branch most easily injured by constriction of the wrist. Its area of innervation can vary widely (see figure). Axonal regeneration of contused nerves proceeds at about l mm per day (or about an inch a month); thus recovery may require two months (measuring from site of injury in wrist to end of area of paresthesia). 

NSAIDs are commonly prescribed. 

In some cases surgical decompression is required(74% success after surgical decompression)- longitudinal incision volar to Tinel's sign,neurolysis and release of fascia between brachioradialis and ECRL.

The efficacy of cortisone and laser treatment is disputed. Permanent damage is possible.

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).