Counter-jihad or Counterjihad or Counter-jihad movement is a political current loosely consisting of authors, bloggers, think tanks, street movements and campaign organisations all linked by a common belief that the Western world is being subjected to takeover by Muslims. Several academic accounts have presented conspiracy theory as a key component of the counter jihad movement.

While the roots of the movement go back to the 1980s, it did not gain significant momentum until after the September 11 attacks in 2001 and the 7 July 2005 London bombings. As far back as 2006, online commentators such as Fjordman were identified as playing a key role in forwarding the nascent counter-jihad ideology. The movement received considerable attention following the 2011 Breivik murders whose manifesto extensively reproduced the writings of prominent counter-jihad bloggers, and following the emergence of prominent street movements such as the English Defence League (EDL). The movement has been variously described as pro-Israel, anti-Islamic, Islamophobic, inciting hatred against Muslims, or far-right.

The movement has adherents both in Europe and in North America, which according to some vary in tone. The European wing is more focused on the alleged cultural threat to European traditions stemming from immigrant Muslim populations, whereas the American wing emphasizes an alleged external threat, essentially terrorist in nature.

The 969 Movement () is a nationalist movement opposed to what they see as Islam’s expansion in predominantly-Buddhist Burma. The three digits of 969 "symbolise the virtues of the Buddha, Buddhist practices and the Buddhist community". The first 9 stands for the nine special attributes of the Lord Buddha and the 6 for the six special attributes of his Dharma, or Buddhist Teachings, and the last 9 represents the nine special attributes of Buddhist Sangha (monastic community). Those special attributes are the Three Jewels of the Buddha. In the past, the Buddha, Sangha, Dhamma, the wheel of Dhamma, and "969" were Buddhist signs.

The movement has inspired strong reactions within and beyond Myanmar. In the international media it has received criticism. "The Straits Times" reported that Ashin Wirathu, the movement's leader, responded to recent anti-Muslim violence with pledges to work for peace but critics remain sceptical.

Various media organizations have described the movement as being anti-Muslim or "Islamophobic". The movement's Myanmar Buddhist supporters deny it is anti-Muslim, with Bhikkhu Wirathu stating it is a protective movement about targeting "Bengalis who are terrorizing ethnic Rakhine (Buddhists)". Alex Bookbinder, in "The Atlantic", links the movement's origins in a book written in the late 1990s by Kyaw Lwin, a functionary in the Ministry of Religious Affairs, and its precepts are rooted in a traditional belief in numerology. Across South Asia, Muslims represent the phrase "In the Name of Allah, the Compassionate and Merciful" with the number 786, and businesses display the number to indicate that they are Muslim-owned. 969's proponents see this as a Muslim plot to conquer Burma in the 21st century, based on the premise that 7 plus 8 plus 6 is equal to 21. The number 969 is intended to be 786's cosmological opposite.

Counter-jihad is a transatlantic "radical right" wing movement which, via "the sharing of ideas between Europeans and Americans and daily linking between blogs and websites on both sides of the Atlantic" "calls for a counterjihad against the supposed Islamisation of Europe".

While the roots of the movement go back to the 1980s, it did not gain significant momentum until after the September 11 attacks in 2001.

The authors of "Right-Wing Populism in Europe: Politics and Discourse" describe the movement as heavily relying on two key tactics. "The first is arguing that the most radical Muslims – men like Osama bin Laden – are properly interpreting the Quran, while peaceful moderate Muslims either do not understand their own holy book or are strategically faking their moderation. The second key tactic is to relentlessly attack individuals and organizations that purport to represent moderate Islam...painting them as secret operatives in a grand Muslim scheme to destroy the West."

Benjamin Lee describes the "counter-jihad scene" as one where "Europe and the United States are under threat from an aggressive and politicized Islamic world that is attempting to take over Europe through a process of "Islamification" with the eventual aim of imposing Sharia law. In this process, the threat is characterized by the perceived removal of Christian or Jewish symbols, the imposition of Islamic traditions, and the creation of no-go areas for non-Muslims. The construction of mosques in particular is seen as continued reinforcement of the separation of the Muslim population from the wider populous. As strong as the threatening practices of Muslims in descriptions of the counter jihad are images of a powerless Europe in decline and sliding into decadence, unable to resist Islamic takeover. The idea that European culture in particular is in a state of decline, while a spiritually vigorous East represented by Islam is in the ascendancy in civil society, is a common sentiment in some circles."

Two central Counter-jihad themes have been identified:

- the notion that Islam poses a threat to "Western civilisation" with a particular focus on "Muslims living in Europe", that is, within the European Counterjihad Movement (ECJM), "seen predominantly in terms of immigration" particularly Muslim immigration.

- a lack of trust in regional, political and economic "elites", with a particular focus against the European Union (EU).

The movement is seeking to draft a law that would forbid Buddhist women from marrying non-Buddhist men without the permission of local officials. Dhammapiya, a senior monk who helped write the original proposal for the laws, said they were meant to encourage peace between different faiths and to "protect" Buddhist women from being forced to convert to Islam when they married Muslim men. Government religious regulatory authorities, while supporting the protection of the Buddhist faith from perceived Islamic threats, reject the legal initiatives of the 969 movement and "prohibited the creation of formal organisations" based on 969 principles.

Stingers are best diagnosed by a medical professional. This person will assess the athlete's pain, range of head and neck motion, arm numbness, and muscle strength. Often, the affected athlete is allowed to return to play within a short time, but persistent symptoms will result in removal. Athletes are also advised to receive

regular evaluations until symptoms have ceased. If they have not after two weeks, or increase, additional tests such as magnetic resonance imaging (MRI) can be performed to detect a more serious injury, such as a herniated disc.

The order of treatments applied depends on whether the athlete's main complaint is pain or weakness. Both can be treated with an analgesic, anti-inflammatory medication, ice and heat, restriction of movement, and if necessary, cervical collar or traction. Surgery is only necessary in the most severe cases.

Stingers can be prevented by wearing protective gear, such as butterfly restrictors, designed to protect the head and neck from being forced into unnatural positions. This equipment is more feasible in positions where unrestricted head and neck movement is not required, such as American football lineman, than in positions like quarterback, where such movement is integral. Regardless of equipment, it is important to report even minor symptoms to an athletic trainer or team physician, and to allow appropriate recovery time.

Protein function tests that demonstrate a reduce in chorein levels and also genetic analysis can confirm the diagnosis given to a patient. For a disease like this it is often necessary to sample the blood of the patient on multiple occasions with a specific request given to the haematologist to examine the film for acanthocytes. Another point is that the diagnosis of the disease can be confirmed by the absence of chorein in the western blot of the erythrocyte membranes.

Impingement syndrome can usually be diagnosed by history and physical exam. On physical exam, the physician may twist or elevate the patient's arm to test for reproducible pain (Neer sign and Hawkins-Kennedy test). These tests help localize the pathology to the rotator cuff; however, they are not specific for impingement. Neer sign may also be seen with subacromial bursitis.

The physician may inject lidocaine (usually combined with a steroid) into the bursa, and if there is an improved range of motion and decrease in pain, this is considered a positive "Impingement Test". It not only supports the diagnosis for impingement syndrome, but it is also therapeutic.

Plain x-rays of the shoulder can be used to detect some joint pathology and variations in the bones, including acromioclavicular arthritis, variations in the acromion, and calcification. However, x-rays do not allow visualization of soft tissue and thus hold a low diagnostic value. Ultrasonography, arthrography and MRI can be used to detect rotator cuff muscle pathology. MRI is the best imaging test prior to arthroscopic surgery. Due to lack of understanding of the pathoaetiology, and lack of diagnostic accuracy in the assessment process by many physicians, several opinions are recommended before intervention.

Imaging features of adhesive capsulitis are seen on non-contrast MRI, though MR arthrography and invasive arthroscopy are more accurate in diagnosis. Ultrasound and MRI can help in diagnosis by assessing the coracohumeral ligament, with a width of greater than 3 mm being 60% sensitive and 95% specific for the diagnosis. The condition can also be associated with edema or fluid at the rotator interval, a space in the shoulder joint normally containing fat between the supraspinatus and subscapularis tendons, medial to the rotator cuff. Shoulders with adhesive capsulitis also characteristically fibrose and thicken at the axillary pouch and rotator interval, best seen as dark signal on T1 sequences with edema and inflammation on T2 sequences. A finding on ultrasound associated with adhesive capsulitis is hypoechoic material surrounding the long head of the biceps tendon at the rotator interval, reflecting fibrosis. In the painful stage, such hypoechoic material may demonstrate increased vascularity with Doppler ultrasound.

Diagnosis of MSA can be challenging because there is no test that can definitively make or confirm the diagnosis in a living patient. Clinical diagnostic criteria were defined in 1998 and updated in 2007. Certain signs and symptoms of MSA also occur with other disorders, such as Parkinson's disease, making the diagnosis more difficult.

Both MRI and CT scanning frequently show a decrease in the size of the cerebellum and pons in those with cerebellar features. The putamen is hypodense on T2-weighted MRI and may show an increased deposition of iron in Parkinsonian form. In cerebellar form, a "hot cross" sign has been emphasized; it reflects atrophy of the pontocereballar fibers that manifest in T2 signal intensity in atrophic pons.

A definitive diagnosis can only be made pathologically on finding abundant glial cytoplasmic inclusions in the central nervous system.

Surgery, such as the denervation of selected muscles, may also provide some relief; however, the destruction of nerves in the limbs or brain is not reversible and should be considered only in the most extreme cases. Recently, the procedure of deep brain stimulation (DBS) has proven successful in a number of cases of severe generalised dystonia. DBS as treatment for medication-refractory dystonia, on the other hand, may increase the risk of suicide in patients. However, reference data of patients without DBS therapy are lacking.

CMM has clear severe impacts on a patient’s ability to carry out daily manual tasks. It is recommended that children be placed under more forgiving school environments, allowing more time for written evaluations and limiting handwritten assignments, to ease the burden of the movement disability. Furthermore, because of patients’ inability to perform pure unilateral movements and their difficulty with tasks requiring skilled bimanual coordination, young and new members to the workforce are encouraged to consider professions that do not require complex bimanual movements, repetitive or sustained hand movements, or extensive handwriting, to reduce overuse, pain, and discomfort in upper limbs.

Because of its pronounced and obviously noticeable signs and symptoms, CMM patients can suffer social stigma, however physicians need to make it clear to parents, family, and friends that the disorder bears no relation to intellectual abilities. However, the rarity of this neurologic disease, found in one in a million people, makes its societal and cultural significance quite limited.

Tullio phenomenon, sound-induced vertigo, dizziness, nausea or eye movement (nystagmus) was first described in 1929 by the Italian biologist Prof. Pietro Tullio. (1881–1941) During his experiments on pigeons, Tullio discovered that by drilling tiny holes in the semicircular canals of his subjects, he could subsequently cause them balance problems when exposed to sound.

The cause is usually a fistula in the middle or inner ear, allowing abnormal sound-synchronized pressure changes in the balance organs. Such an opening may be caused by a barotrauma (e.g. incurred when diving or flying), or may be a side effect of fenestration surgery, syphilis or Lyme disease.

Patients with this disorder may also experience vertigo, imbalance and eye movement set off by changes in pressure, e.g. when nose-blowing, swallowing or when lifting heavy objects.

Tullio phenomenon is also one of the common symptoms of superior canal dehiscence syndrome (SCDS), first diagnosed in 1998 by Dr. Lloyd B. Minor, The Johns Hopkins University, Baltimore, United States.

In terms of selective muscle weakness or poor flexibility muscular imbalance is frequently regarded as an etiological factor in the onset of musculoskeletal disorders. There are a variety of areas that can be affected, each causing different symptoms hence there are also different treatments available, but in general cases muscle strengthening techniques were developed for the use on the weak or tight muscles.

Diagnosis consists of a variety of tests, including but not limited to:

- Measurement of orthostatic blood pressure

- Coordination

- rapid, alternating movements

- stroking of heel from along the opposite shin from knee to ankle

- finger-to-nose testing.

- Primary sensory modalities are examined with the following methods, searching for focal sensory loss, graded distal sensory loss, or levels of decreased sensation, hyperesthesia or dysesthesia.

- light touch

- pin-prick

- temperature

- position

- vibration

- Focused gait examination, which examines stationary position and walking abnormalities. Walking generally exposes any faults within the complex neurological communication between systems as weight is shifted from one foot to the other.

Treatment consists of physical rehabilitation programs designed to improve overall function, increase strength and improve balance. The ultimate goal is to increase the patient's degree of independence, thus improving the patient's quality of life. Exercise typically begins with simple movements, gradually transitioning into more complex actions. Various aspects of treatment are assessed based on the individual patient's condition, utilizing many assessment tools:

- Functional Reach Test

- External Perturbation Test – Push, Release

- External Perturbation Test – Pull

- Clinical Sensory Integration Test

- Single Leg Stance Test

- Five Times Sit to Stand Test

Various scales are also utilized

- Brief Ataxia Rating Scale

- Friedreich's Ataxia Impact Scale

- Scale For Assessment and Rating of Ataxia

Although treatment for tennis elbow prior 2010 was unknown because the etiology remained unclear, tests confirmed that the cause was an imbalance with the agonist-antagonist functional relationship. Treatment now includes anti-inflammatory medicines, rest, equipment check, physical therapy, braces, steroid injections, shock wave therapy and if symptoms persist after 6 to 12 months, doctors may recommend surgery.

Although treatment varies depending on how bad eye alignment is and also the underlying causes of strabismus. Treatment for strabismus may include orthoptics a term used for eye muscle training, this treatment can be provided by orthoptists and also optometrists. Other treatment may include wearing eye patches aimed at strengthening the weaker eye while inhibiting the stronger eye, an alternative to eye patches is the use of an opaque lens, other treatments may include eye drops to temporarily inhibit the stronger eye and at any age eye muscle surgery can be done to correct the muscular balance of the ocular muscles.

Although the cause of scoliosis can sometimes remain unknown (idiopathic scoliosis) there is treatment available that targets at strengthening the back muscles, for milder cases usually do not require medical attention, more severe cases require either muscle strengthening exercises aimed at the back muscles and even special back braces or surgery can be recommended if the case is extreme. Studies have shown that treatment with a special back brace among children ranging from 10–16 years can be successful and using this method of muscle training scoliosis can be cured with non-surgical treatment.

To prevent the problem, a common recommendation is to keep the shoulder joint fully moving to prevent a frozen shoulder. Often a shoulder will hurt when it begins to freeze. Because pain discourages movement, further development of adhesions that restrict movement will occur unless the joint continues to move full range in all directions (adduction, abduction, flexion, rotation, and extension). Physical therapy and occupational therapy can help with continued movement.

Diagnosis is made on the basis of the association of gastro-oesophageal reflux with the characteristic movement disorder. Neurological examination is usually normal. Misdiagnosis as benign infantile spasms or epileptic seizures is common, particularly where clear signs or symptoms of gastro-oesophageal reflux are not apparent. Early diagnosis is critical, as treatment is simple and leads to prompt resolution of the movement disorder.

Currently, clinical diagnosis of CMM disorder has been based on clinical findings or molecular genetic testing.

"Clinical Findings (Signs and Symptoms)"""":"

- onset of mirror movements in infancy or early childhood

- persistence of mirror movements into and throughout adulthood with the absence of other neurologic disorders

- little improvement nor deterioration of mirror movements over the course of one’s life

- intensity of mirrored movements increasing with the complexity of the voluntary movement

- involuntary mirror movements that are generally of lesser amplitude compared with voluntary movements

- predominant mirror movement in upper limbs, with increasing severity in more distal appendages (fingers)

- inability to perform tasks requiring skilled bimanual coordination

- occasional pain in the upper limbs during prolonged manual activities

- occasional observed subclinical mirroring movement, but detectable with accelerometer gloves

"Molecular genetic testing"":"

- identification of a heterozygous mutant "DCC, DNAL4, or RAD51" gene (single gene test or multi-gene panel)

In May 2013, the US FDA granted Orphan drug status to Diiodothyropropionic acid (DITPA) in the treatment of MCT8 deficiency. This was following the use of DITPA towards a child in Australia, under compassionate grounds.

There is no established treatment for AHDS. Theoretical considerations suggested TRIAC (triiodothyroacetate or tiratricol, a natural non-classical thyroid hormone) to be beneficial. In 2014, a case was demonstrated in which therapy with TRIAC in early childhood led to significant improvement of cognition and mobility. Currently, the effect of Triac is under investigation.

Step I : Decide the dominant type of movement disorder

Step II : Make differential diagnosis of the particular disorder

Step II: Confirm the diagnosis by lab tests

- Metabolic screening

- Microbiology

- Immunology

- CSF examination

- Genetics

- Imaging

- Neurophysiological tests

- Pharmacological tests

MSA usually progresses more quickly than Parkinson's disease. There is no remission from the disease. The average remaining lifespan after the onset of symptoms in patients with MSA is 7.9 years. Almost 80% of patients are disabled within five years of onset of the motor symptoms, and only 20% survive past 12 years. Rate of progression differs in every case and speed of decline may vary widely in individual patients.

O’Sullivan and colleagues (2008) identified early autonomic dysfunction to be the most important early clinical prognostic feature regarding survival in MSA. Patients with concomitant motor and autonomic dysfunction within three years of symptom onset had a shorter survival duration, in addition to becoming wheelchair dependent and bed-ridden at an earlier stage than those who developed these symptoms after three years from symptom onset. Their study also showed that when patients with early autonomic dysfunction develop frequent falling, or wheelchair dependence, or severe dysphagia, or require residential care, there is a shorter interval from this point to death.

In the past, the prognosis for patients with this disease had been very poor; with many patients suffering from severe disability or death. Now, patients are responding remarkably well to current treatments and the majority of patients go into spontaneous remission. For those that do not go into remission, the symptoms of hemiballismus can generally be very well controlled with medication.

Due to the rarity of this disorder, scientists know very little about the details of hemiballismus. There are still many unanswered questions such as:

•There appears to be a discrepancy between this disorder in humans and animals that has yet to be explained.

•Hemiballismus can also be induced by damage to other areas of the basal ganglia besides the subthalamic nucleus. Why is this? Research is being done in these areas in order to give scientists and clinicians a better model for this disease that will ultimately lead to better diagnosis and treatment of this disorder.

•Research is also being done on why certain treatments seem to help hemiballistic patients when they should seemingly do more harm. An example of this is why lesioning the globus pallidus seems to reduce hemiballistic movements.

•Why does blocking dopamine help reduce patients’ symptoms?

The physical characteristics of the tremor and the history of the patient will contribute to the diagnosis of Holmes tremor. A doctor will determine if the tremor is present during rest or voluntary muscle contraction and the frequency of the tremor. A Holmes tremor is generally made worse upon standing and upon intentional movements. Also, a Holmes tremor is not as rhythmic as other tremors.

To confirm the diagnosis of a Holmes tremor, a doctor will usually perform ancillary examinations. This includes measuring serum thyroid stimulating hormone levels to ensure the thyroid is functioning normally. This rules out the possibility hyperthyroidism is causing a different type of tremor. An MRI can also be performed to look for structural lesions in areas such as the thalamus, midbrain tegmentum, and substantia nigra.