A doctor will base his or her diagnosis on the symptoms the patient has and the results of tests, including:

- An X-ray

- Magnetic resonance imaging (MRI), which usually provides the most information

- Computed tomography (CT) scan

If there aren't neurological symptoms (such as difficulties moving, loss of sensation, confusion, etc.) and there is no evidence of pressure on the spinal cord, a conservative approach may be taken such as:

- Drugs, such as aspirin, without steroids to relieve inflammation

- Cervical traction, in which the neck is pulled along its length, thus relieving pressure on the spinal cord

- Using a neck collar or cervical-thoracic suit

If there is pressure on the spinal cord or life-threatening symptoms are present, surgery is recommended.

A combination of lifestyle modifications and medications can be used for the treatment of dolichoectasias.

- Antihypertensive medications such as Thiazides, Beta Blocker, ACE Inhibitor

- Trental or other Pentoxifylline drugs

- Dietary changes

- Weight loss

- Regular exercise

During the early stage, an x-ray will not be helpful because there is no calcium in the matrix. (In an acute episode which is not treated, it will be 3– 4 weeks after onset before the x-ray is positive.) Early laboratory tests are not very helpful. Alkaline phosphatase will be elevated at some point, but initially may be only slightly elevated, rising later to a high value for a short time. Unless weekly tests are done, this peak value may not be detected. It is not useful in patients who have had fractures or spine fusion recently, as they will cause elevations.

The only definitive diagnostic test in the early acute stage is a bone scan, which will show hetertopic ossification 7 – 10 days earlier than an x-ray. The three-phase bone scan may be the most sensitive method of detecting early heterotopic bone formation. However, an abnormality detected in the early phase may not progress to the formation of heterotopic bone. Another finding, often misinterpreted as early heterotopic bone formation, is an increased (early) uptake around the knees or the ankles in a patient with a very recent spinal cord injury. It is not clear exactly what this means, because these patients do not develop heterotopic bone formation. It has been hypothesized that this may be related to the autonomic nervous system and its control over circulation.

When the initial presentation is swelling and increased temperature in a leg, the differential diagnosis includes thrombophlebitis. It may be necessary to do both a bone scan and a venogram to differentiate between heterotopic ossification and thrombophlebitis, and it is even possible that both could be present simultaneously. In heterotopic ossification, the swelling tends to be more proximal and localized, with little or no foot/ankle edema, whereas in thrombophlebitis the swelling is usually more uniform throughout the leg.

Benign fasciculation syndrome is a diagnosis of exclusion; that is, other potential causes for the twitching (mostly forms of neuropathy or motor neuron diseases such as ALS) must be ruled out before BFS can be assumed. An important diagnostic tool here is electromyography (EMG). Since BFS appears to cause no actual nerve damage (at least as seen on the EMG), patients will likely exhibit a completely normal EMG (or one where the only abnormality seen is fasciculations).

Another important step in diagnosing BFS is checking the patient for clinical weakness. Clinical weakness is often determined through a series of strength tests, such as observing the patient's ability to walk on his or her heels and toes. Resistance strength tests may include raising each leg, pushing forward and backward with the foot and/or toes, squeezing with fingers, spreading fingers apart, and pushing with or extending arms and/or hands. In each such test the test provider will apply resisting force and monitor for significant differences in strength abilities of opposing limbs or digits. If such differences are noted or the patient is unable to apply any resisting force, clinical weakness may be noted.

Lack of clinical weakness along with normal EMG results (or those with only fasciculations) largely eliminates more serious disorders from potential diagnosis.

Especially for younger persons who have only LMN sign fasciculations, "In the absence of weakness or abnormalities of thyroid function or electrolytes, individuals under 40 years can be reassured without resorting to electromyography (EMG) to avoid the small but highly damaging possibility of false-positives". "Equally, however, most subspecialists will recall a small number of cases, typically men in their 50s or 60s, in whom the latency from presentation with apparently benign fasciculations to weakness (and then clear MND) was several years. Our impression is that a clue may be that the fasciculations of MND are often abrupt and widespread at onset in an individual previously unaffected by fasciculations in youth. The site of the fasciculations, for example, those in the calves versus abdomen, has not been shown to be discriminatory for a benign disorder. There is conflicting evidence as to whether the character of fasciculations differs neurophysiologically in MND".

Another abnormality commonly found upon clinical examination is a brisk reflex action known as "hyperreflexia". Standard laboratory tests are unremarkable. According to neurologist John C. Kincaid:

Treatment involves removal of the etiologic mass and decompressive craniectomy. Brain herniation can cause severe disability or death. In fact, when herniation is visible on a CT scan, the prognosis for a meaningful recovery of neurological function is poor. The patient may become paralyzed on the same side as the lesion causing the pressure, or damage to parts of the brain caused by herniation may cause paralysis on the side opposite the lesion. Damage to the midbrain, which contains the reticular activating network which regulates consciousness, will result in coma. Damage to the cardio-respiratory centers in the medulla oblongata will cause respiratory arrest and (secondarily) cardiac arrest. Current investigation is underway regarding the use of neuroprotective agents during the prolonged post-traumatic period of brain hypersensitivity associated with the syndrome.

Brain herniation frequently presents with abnormal posturing a characteristic positioning of the limbs indicative of severe brain damage. These patients have a lowered level of consciousness, with Glasgow Coma Scores of three to five. One or both pupils may be dilated and fail to constrict in response to light. Vomiting can also occur due to compression of the vomiting center in the medulla oblongata.

There is no clear form of treatment. Originally, bisphosphonates were expected to be of value after hip surgery but there has been no convincing evidence of benefit, despite having been used prophylactically.

Depending on the growth's location, orientation and severity, surgical removal may be possible.

Radiation Therapy.

Prophylactic radiation therapy for the prevention of heterotopic ossification has been employed since the 1970s. A variety of doses and techniques have been used. Generally, radiation therapy should be delivered as close as practical to the time of surgery. A dose of 7-8 Gray in a single fraction within 24–48 hours of surgery has been used successfully. Treatment volumes include the peri-articular region, and can be used for hip, knee, elbow, shoulder, jaw or in patients after spinal cord trauma.

Single dose radiation therapy is well tolerated and is cost effective, without an increase in bleeding, infection or wound healing disturbances.

Other possible treatments.

Certain antiinflammatory agents, such as indomethacin, ibuprofen and aspirin, have shown some effect in preventing recurrence of heterotopic ossification after total hip replacement.

Conservative treatments such as passive range of motion exercises or other mobilization techniques provided by physical therapists or occupational therapists may also assist in preventing HO. A review article looked at 114 adult patients retrospectively and suggested that the lower incidence of HO in patients with a very severe TBI may have been due to early intensive physical and occupational therapy in conjunction with pharmacological treatment. Another review article also recommended physiotherapy as an adjunct to pharmacological and medical treatments because passive range of motion exercises may maintain range at the joint and prevent secondary soft tissue contractures, which are often associated with joint immobility.

Foville's syndrome is caused by the blockage of the perforating branches of the basilar artery in the region of the brainstem known as the pons. Most frequently caused by vascular disease or tumors involving the dorsal pons.[3]

Structures affected by the infarct are the PPRF, nuclei of cranial nerves VI and VII, corticospinal tract, medial lemniscus, and the medial longitudinal fasciculus. There's involvement of the fifth to eighth cranial nerves, central sympathetic fibres (Horner syndrome) and horizontal gaze palsy.[3]

Evidence does not support the use of preventative antibiotics regardless of the presence of a cerebral spinal fluid leak.

The term dolichoectasia means elongation and distension. It is used to characterize arteries throughout the human body which have shown significant deterioration of their tunica intima (and occasionally the tunica media), weakening the vessel walls and causing the artery to elongate and distend.

Some degree of control of the fasciculations may be achieved with the same medication used to treat essential tremor (beta-blockers and anti-seizure drugs). However, often the most effective approach to treatment is to treat any accompanying anxiety. No drugs, supplements, or other treatments have been found that completely control the symptoms. In cases where fasciculations are caused by magnesium deficiency, supplementing magnesium can be effective in reducing symptoms.

In many cases, the severity of BFS symptoms can be significantly reduced through a proactive approach to decrease the overall daily stress. Common ways to reduce stress include: exercising more, sleeping more, working less, meditation, and eliminating all forms of dietary caffeine (e.g. coffee, chocolate, cola, and certain over-the counter medications).

If pain or muscle aches are present alongside fasciculations, patients may be advised to take over-the-counter pain medications such as ibuprofen or acetaminophen during times of increased pain. Other forms of pain management may also be employed. Prior to taking any over-the-counter medications, individuals should initiate discussions with their health care provider(s) to avoid adverse effects associated with long-term usage or preexisting conditions.

A urologist may be able to diagnose the disease and suggest treatment. An ultrasound can provide conclusive evidence of Peyronie's disease, ruling out congenital curvature or other disorders.

Different features of the dysostosis are significant. Radiological imaging helps confirm the diagnosis. During gestation (pregnancy), clavicular size can be calculated using available nomograms. Wormian bones can sometimes be observed in the skull.

Diagnosis of CCD spectrum disorder is established in an individual with typical clinical and radiographic findings and/or by the identification of a heterozygous pathogenic variant in RUNX2 (CBFA1).

Non-displaced fractures usually heal without intervention. Patients with basilar skull fractures are especially likely to get meningitis. Unfortunately, the efficacy of prophylactic antibiotics in these cases is uncertain.

This produces ipsilateral horizontal gaze palsy and facial nerve palsy and contralateral hemiparesis, hemisensory loss, and internuclear ophthalmoplegia.

Macroglossia is usually diagnosed clinically. Sleep endoscopy and imaging may be used for assessment of obstructive sleep apnea. The initial evaluation of all patients with macroglossia may involve abdominal ultrasound and molecular studies for Beckwith–Wiedemann syndrome.

Benedikt syndrome, also called Benedikt's syndrome or paramedian midbrain syndrome, is a rare type of posterior circulation stroke of the brain, with a range of neurological symptoms affecting the midbrain, cerebellum and other related structures.

Treatment of migraine-associated vertigo is the same as the treatment for migraine in general.

Medial inferior pontine syndrome is a condition associated with a contralateral hemiplegia.

"Medial inferior pontine syndrome" has been described as equivalent to Foville's syndrome.

Deep brain stimulation may provide relief from some symptoms of Benedikt syndrome, particularly the tremors associated with the disorder.

Hemotympanum or hematotympanum, refers to the presence of blood in the tympanic cavity of the middle ear. Hemotympanum is often the result of basilar skull fracture.

Although medial pontine syndrome has many similarities to medial medullary syndrome, because it is located higher up the brainstem in the pons, it affects a different set of cranial nuclei.

Depending upon the size of the infarct, it can also involve the facial nerve.

MAV is not recognized as a distinct diagnostic entity. Lembert and Neuhauser propose criteria for definite and probable migraine-associated vertigo.

A diagnosis of "definite migraine-associated vertigo" includes a case history of:

- episodic vestibular symptoms of at least moderate severity;

- current or previous history of migraine according to the 2004 "International Classification of Headache Disorders";

- one of the following migrainous symptoms during two or more attacks of vertigo: migrainous headache, photophobia, phonophobia, visual or other auras; and

- other causes ruled out by appropriate investigations.

A diagnosis of "probable migraine-associated vertigo" includes a case history of episodic vestibular symptoms of at least moderate severity and one of the following:

- current or previous history of migraine according to the 2004 "International Classification of Headache Disorders";

- migrainous symptoms during vestibular symptoms;

- migraine precipitants of vertigo in more than 50% of attacks, such as food triggers, sleep irregularities, or hormonal change;

- response to migraine medications in more than 50% of attacks; and

- other causes ruled out by appropriate investigations.

Note that, in both of the above criteria, headache is not required to make the diagnosis of migraine-associated vertigo.

They add that, in patients with a clear-cut history, no vestibular tests are required. Other historical criteria which are helpful in making the diagnosis of migraine-associated vertigo are vertiginous symptoms throughout the patient’s entire life, a long history of motion intolerance, sensitivity to environmental stimuli, illusions of motion of the environment, and vertigo that awakens the patient.

Prevalence is estimated to be 0.005%. The age of onset has been found to be under 15 years in 40% of cases while it is between 10 and 14 years in one third of the cases. Females outnumber males, 4 to 1. Only 3% have attacks after age 52.