Hemicrania continua generally responds only to indomethacin 25–300 mg daily, which must be continued long term. Unfortunately, gastrointestinal side effects are a common problem with indomethacin, which may require additional acid-suppression therapy to control.

In patients who are unable to tolerate indomethacin, the use of celecoxib 400–800 mg per day (Celebrex) and rofecoxib 50 mg per day (Vioxx - no longer available) have both been shown to be effective and are likely to be associated with fewer GI side effects. There have also been reports of two patients who were successfully managed with topiramate 100–200 mg per day (Topamax) although side effects with this treatment can also prove problematic.

Greater Occipital Nerve [GON] block comprising 40 mg Depomedrone and 10mls of 1% Lignocaine injected into the affected nerve is effective, up to a period of approximately three months. Changing the 'cocktail' to include [for example] 10mls of .5% Marcaine and changing to 2% Lignocaine, whilst in theory should increase the longevity, renders the injection completely ineffective. See 4.2 Posology and method of administration [flocculation]

Occipital nerve stimulation may be highly effective when other treatments fail to relieve the intractable pain.

Though outwardly similar to cluster headaches, chronic paroxysmal hemicrania is rather different, and the two headaches are not a subset of one or the other. Key differences include:

- Different gender distributions – CPH is more common in women than men, with opposite occurring with cluster headaches.

- CPH attacks occur more frequently, but are shorter.

- Individuals with CPH are far more responsive to indomethacin than individuals with cluster headaches.

- CPH attacks can be provoked by neck movement.

- In a study conducted by Sjaastad, heating a patient's body will cause the painful side of the forehead to sweat more in CPH patients, while there will be less sweating on that side for those suffering from cluster headaches.

A ten-patient study conducted by Pareja et al. found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. Doses of the drug ranged from 25 mg per day to 150 mg per day with a median dose of 75 mg per 24-hour period.

Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued use of the drug due to adverse side effects, namely complications in the gastrointestinal tract.

According to a case study by Milanlioglu et al., 100mg of lamotrigine, an antiepileptic drug, administered twice daily alleviated all painful symptoms. No side effects were noted after two months of treatment. Dosage of lamotrigine was decreased to 50mg a day after the first two months, and no symptoms or side-effects were recorded after a three-month followup.

Use of topiramate has also been found to be an effective treatment for CPH, but cluster headache medications have been found to have little effect.

Cluster headaches are often misdiagnosed, mismanaged, or undiagnosed for many years; they may be confused with migraine, "cluster-like" headache (or mimics), CH subtypes, other TACs ( trigeminal autonomic cephalalgias), or other types of primary or secondary headache syndrome. Cluster-like head pain may be diagnosed as secondary headache rather than cluster headache.

A detailed oral history aids practitioners in correct differential diagnosis, as there are no confirmatory tests for CH. A headache diary can be useful in tracking when and where pain occurs, how severe it is, and how long the pain lasts. A record of coping strategies used may help distinguish between headache type; data on frequency, severity and duration of headache attacks are a necessary tool for initial and correct differential diagnosis in headache conditions.

Correct diagnosis presents a challenge as the first CH attack may present where staff are not trained in the diagnosis of rare or complex chronic disease. Although experienced ER staff are sometimes trained to detect headache types, CH attacks themselves are not directly life-threatening, they are linked to an increased risk of suicide.

Individuals with CH typically experience diagnostic delay before correct diagnosis. People are often misdiagnosed due to reported neck, tooth, jaw, and sinus symptoms and may unnecessarily endure many years of referral to ear, nose and throat (ENT) specialists for investigation of sinuses; dentists for tooth assessment; chiropractors and manipulative therapists for treatment; or psychiatrists, psychologists and other medical disciplines before their headaches are correctly diagnosed. Under-recognition of CH by health care professionals is reflected in consistent findings in Europe and the United States that the average time to diagnosis is around seven years. Medical students receive little training in differential diagnoses and management of headaches.

Cluster headache may be misdiagnosed as migraine or sinusitis. Other types of headache are sometimes mistaken for, or may mimic closely, CH. Incorrect terms like "cluster migraine" confuse headache types, confound differential diagnosis and are often the cause of unnecessary diagnostic delay, ultimately delaying appropriate specialist treatment.

Headaches that may be confused with CH include:

- Chronic paroxysmal hemicrania (CPH) is a unilateral headache condition, without the male predominance usually seen in CH. Paroxysmal hemicrania may also be episodic but the episodes of pain seen in CPH are usually shorter than those seen with cluster headaches. CPH typically responds "absolutely" to treatment with the anti-inflammatory drug indomethacin where in most cases CH typically shows no positive indomethacin response, making "Indomethacin response" an important diagnostic tool for specialist practitioners seeking correct differential diagnosis between the conditions.

- Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT) is a headache syndrome belonging to the group of TACs.

- Trigeminal neuralgia is a unilateral headache syndrome, or "cluster-like" headache.

A lumbar puncture is a procedure in which cerebral spinal fluid is removed from the spine with a needle. A lumbar puncture is necessary to look for infection or blood in the spinal fluid. A lumbar puncture can also evaluate the pressure in the spinal column, which can be useful for people with idiopathic intracranial hypertension (usually young, obese women who have increased intracranial pressure), or other causes of increased intracranial pressure. In most cases, a CT scan should be done first.

The cause of hemicrania continua is unknown. There is no definitive diagnostic test for hemicrania continua. Diagnostic tests such as imaging studies may be ordered to rule out other causes for the headache. When the symptoms of hemicrania continua are present, it's considered "diagnostic" if they respond completely to indomethacin. The efficacy of indomethacin may not be long term for all patients, as can eventually become ineffective.

The factor that allows hemicrania continua and its exacerbations to be differentiated from migraine and cluster headache is that hemicrania continua is completely responsive to indomethacin. Triptans and other abortive medications do not affect hemicrania continua.

All people who present with red flags indicating a dangerous secondary headache should receive neuroimaging. The best form of neuroimaging for these headaches is controversial. Non-contrast computerized tomography (CT) scan is usually the first step in head imaging as it is readily available in Emergency Departments and hospitals and is cheaper than MRI. Non-contrast CT is best for identifying an acute head bleed. Magnetic Resonance Imaging (MRI) is best for brain tumors and problems in the posterior fossa, or back of the brain. MRI is more sensitive for identifying intracranial problems, however it can pick up brain abnormalities that are not relevant to the person's headaches.

The American College of Radiology recommends the following imaging tests for different specific situations:

As diagnostic criteria have been indecisive and its pathophysiology remains unclear, no permanent cure is available. Antiepileptic medications (membrane-stabilizing drugs) such as pregabalin, gabapentin, topiramate, and lamotrigine improve symptoms, but there is no effective permanent or long-term treatment for SUNCT.

However, a few short-term treatments are available and can relieve and possibly prevent some symptoms of attacks.

Lamotrigine exhibits some long-term prevention and reduction in many patients; however, titration of dose is difficult due to adverse skin reactions.

Topiramate also has preventive effects but it is accompanied by a high risk of severe side-effects for patients with a history of kidney stones, glaucoma, depression, or low body weight.

Intravenous lidocaine can abolish symptoms during its administration, or reduce frequency and duration of attacks. However, administration of intravenous lidocaine requires careful monitoring of ECG and blood pressure.

Methylprednisolone therapy shows some promise in short-term prevention of attacks, even though its mechanism of action is yet to be discovered.

The calcium channel blocker verapamil is reported to be useful in alleviating symptoms (lower frequency and duration of attacks), even though some patients experience worsened symptoms.

Various medications that are often used in other headache syndromes such as nonsteroidal anti-inflammatory drugs, acetaminophen, tricyclic antidepressants, calcium channel antagonists do not relieve the symptoms of SUNCT.

There have been attempts to alter oxygen supply during attacks to alleviate the symptoms since some of the headaches are caused by decreased oxygen supply; however, elevated blood oxygen level did not affect the symptoms.

Researchers now focus on the administration of various combination of medications and therapies to treat symptoms of SUNCT.

SUNCT must be properly distinguished from cluster headaches, since cluster headaches also occur several times per day with separate attacks, and share some common symptoms. However, cluster headaches usually last longer (up to three hours), occur less often (three to five attacks per day), and do not accompany cranial autonomic symptoms. IHS standard criteria for the diagnosis of SUNCT specifically includes pain in the trigeminal division of the face, especially in the orbital region, often with cranial autonomic symptoms which last for relatively short periods of time (from five seconds to several minutes) up to 100 times per day. SUNCT is a major subset of SUNA, which does not accompany cranial symptoms; complete separation between the two is inappropriate since SUNCT does not necessarily always accompany cranial autonomic signs. Exact statistical data is not available due to common mis-diagnosis, and setting up diagnostic criteria is important.

The International Headache Classification established by the International Headache Society criteria for diagnosing SUNCT for therapeutic purposes is:

Symptoms of SUNCT often lead to misdiagnosis as paroxysmal hemicrania, which is also categorized in the same group. Inefficiency of indomethacin usually indicates SUNCT over paroxysmal hemicrania.

Misdiagnosis and indecisive diagnosis in the past has made it difficult to obtain accurate statistics about SUNCT. Proper diagnosis will broaden data availability and facilitate discovery of new treatment options and useful statistics.

Preventive treatments of migraines include medications, nutritional supplements, lifestyle alterations, and surgery. Prevention is recommended in those who have headaches more than two days a week, cannot tolerate the medications used to treat acute attacks, or those with severe attacks that are not easily controlled.

The goal is to reduce the frequency, painfulness, and/or duration of migraines, and to increase the effectiveness of abortive therapy. Another reason for prevention is to avoid medication overuse headache. This is a common problem and can result in chronic daily headache.

Long term prognosis in people with migraines is variable. Most people with migraines have periods of lost productivity due to their disease; however typically the condition is fairly benign and is not associated with an increased risk of death. There are four main patterns to the disease: symptoms can resolve completely, symptoms can continue but become gradually less with time, symptoms may continue at the same frequency and severity, or attacks may become worse and more frequent.

Migraines with aura appear to be a risk factor for ischemic stroke doubling the risk. Being a young adult, being female, using hormonal birth control, and smoking further increases this risk. There also appears to be an association with cervical artery dissection. Migraines without aura do not appear to be a factor. The relationship with heart problems is inconclusive with a single study supporting an association. Overall however migraines do not appear to increase the risk of death from stroke or heart disease. Preventative therapy of migraines in those with migraines with auras may prevent associated strokes. People with migraines, particularly women, may develop higher than average numbers of white matter brain lesions of unclear significance.

Trigeminal autonomic cephalgia (TAC) is the name for a type of primary headache that occurs with pain on one side of the head in the trigeminal nerve area and symptoms in autonomic systems on the same side, such as eye watering and redness or drooping eyelids. TACs include

- Cluster headache

- Paroxysmal hemicrania (chronic or episodic)

- Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)

- Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA)

- Long-lasting autonomic symptoms with hemicrania (LASH)

TACs can be differentiated by the length and frequency of recurrence of the headaches.

Treatment for TACs varies depending on the exact type, but can include medication such as Indomethacin (in the case of chronic paroxysmal hemicrania) or acute and prophylactic therapy (in the case of cluster headache).

Hypnic headaches are benign primary headaches that affect the elderly, with the average age of onset being 63 ± 11 years. They are moderate, throbbing, bilateral or unilateral headaches that wake the sufferer from sleep once or multiple times a night. They typically begin a few hours after sleep begins and can last from 15–180 min. There is normally no nausea, photophobia, phonophobia or autonomic symptoms associated with the headache. They commonly occur at the same time every night possibly linking the headaches with circadian rhythm, but polysomnography has recently revealed that the onset of hypnic headaches may be associated with REM sleep.

Lithium carbonate 200–600 mg at bedtime is an effective treatment for most patients but for those that can not tolerate Lithium, Verapamil, indomethacin or methylsergilide may be tried. Two patients have also responded to flunarizine 5 mg. It has also been shown that 1–2 cups of coffee or 100–200 mg of caffeine before bed can prevent hypnic headaches.

For diagnosis of hypnic headache syndrome, headaches should occur at least 15 times per month for at least one month. Included in the differential diagnosis of a new onset nighttime headaches in the elderly is drug withdrawal, temporal arteritis, Sleep apnea, oxygen desaturated, Pheochromocytoma, intracranial causes, primary and secondary neoplasms, communicating hydrocephalus, subdural hematoma, vascular lesions, migraines, cluster headaches, chronic paroxysmal hemicrania and hypnic headache. All other causes must be ruled out before the diagnosis of hypnic headache can be made.

The diagnosis may be made on the clinical features alone, along with tests to rule out other possible causes. An EEG will usually show the electrical features of epilepsy and slowing of brain activity in the affected hemisphere, and MRI brain scans will show gradual shrinkage of the affected hemisphere with signs of inflammation or scarring.

Brain biopsy can provide very strong confirmation of the diagnosis, but this is not always necessary.

During the acute stage, treatment is aimed at reducing the inflammation. As in other inflammatory diseases, steroids may be used first of all, either as a short course of high-dose treatment, or in a lower dose for long-term treatment. Intravenous immunoglobulin is also effective both in the short term and in the long term, particularly in adults where it has been proposed as first-line treatment. Other similar treatments include plasmapheresis and tacrolimus, though there is less evidence for these. None of these treatments can prevent permanent disability from developing.

During the residual stage of the illness when there is no longer active inflammation, treatment is aimed at improving the remaining symptoms. Standard anti-epileptic drugs are usually ineffective in controlling seizures, and it may be necessary to surgically remove or disconnect the affected cerebral hemisphere, in an operation called hemispherectomy. This usually results in further weakness, hemianopsia and cognitive problems, but the other side of the brain may be able to take over some of the function, particularly in young children. The operation may not be advisable if the left hemisphere is affected, since this hemisphere contains most of the parts of the brain that control language. However, hemispherectomy is often very effective in reducing seizures.

MDDS is diagnosed based on systemic symptoms presenting in infants, followed by a clinical examination and laboratory tests (for example, high lactate levels are common) medical imaging, and usually is finally confirmed and formally identified by genetic testing.

Between 10 and 30% of people who have status epilepticus die within 30 days. The great majority of these people have an underlying brain condition causing their status seizure such as brain tumor, brain infection, brain trauma, or stroke. However, people with diagnosed epilepsy who have a status seizure also have an increased risk of death if their condition is not stabilized quickly, their medication and sleep regimen adapted and adhered to, and stress and other stimulant (seizure trigger) levels controlled.

However, with optimal neurological care, adherence to the medication regimen, and a good prognosis (no other underlying uncontrolled brain or other organic disease), the person—even people who have been diagnosed with epilepsy—in otherwise good health can survive with minimal or no brain damage, and can decrease risk of death and even avoid future seizures.

Definitions vary, but currently it is defined as one continuous, unremitting seizure lasting longer than five minutes, or recurrent seizures without regaining consciousness between seizures for greater than five minutes. Previous definitions used a 30-minute time limit.

NCSE is believed to be under-diagnosed.

DGUOK, POLG, and MPV17 related forms result in defects to the liver. Liver dysfunction is progressive in the majority of individuals with both forms of DGUOK-related MDS and is the most common cause of death. For children with the multi-organ form, liver transplantation provides no survival benefit.

Liver disease typically progresses to liver failure in affected children with MPV17-related MDS and liver transplantation remains the only treatment option for liver failure. Approximately half of affected children reported did not undergo liver transplantation and died because of progressive liver failure – the majority during infancy or early childhood. A few children were reported to survive without liver transplantation.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

Pituitary incidentalomas are pituitary tumors that are characterized as an incidental finding. They are often discovered by computed tomography (CT) or magnetic resonance imaging (MRI), performed in the evaluation of unrelated medical conditions such as suspected head trauma, in cancer staging or in the evaluation of nonspecific symptoms such as dizziness and headache. It is not uncommon for them to be discovered at autopsy. In a meta-analysis, adenomas were found in an average of 16.7% in postmortem studies, with most being microadenomas (<10mm); macrodenomas accounted for only 0.16% to 0.2% of the decedents. While non-secreting, noninvasive pituitary microadenomas are generally considered to be literally as well as clinically benign, there are to date scant studies of low quality to support this assertion.

It has been recommended in the current Clinical Practice Guidelines (2011) by the Endocrine Society - a professional, international medical organization in the field of endocrinology and metabolism - that all patients with pituitary incidentalomas undergo a complete medical history and physical examination, laboratory evaluations to screen for hormone hypersecretion and for hypopituitarism. If the lesion is in close proximity to the optic nerves or optic chiasm, a visual field examination should be performed. For those with incidentalomas which do not require surgical removal, follow up clinical assessments and neuroimaging should be performed as well follow-up visual field examinations for incidentalomas that abut or compress the optic nerve and chiasm and follow-up endocrine testing for macroincidentalomas.

Dermatitis repens (also known as "Acrodermatitis continua," "Acrodermatitis perstans," "Pustular acrodermatitis," "Acrodermatitis continua of Hallopeau," "Acrodermatitis continua suppurativa Hallopeau," "Hallopeau's acrodermatitis,", "Hallopeau's acrodermatitis continua," and "Dermatitis repens Crocker") is a rare, sterile, pustular eruption of the fingers and toes that slowly extends proximally.

Localized pustular psoriasis presents as two distinct conditions that must be considered separate from generalized psoriasis, and without systemic symptoms, these two distinct varieties being pustulosis palmaris et plantaris and acrodermatitis continua.

Cases of epilepsy may be organized into epilepsy syndromes by the specific features that are present. These features include the age at which seizures begin, the seizure types, and EEG findings, among others. Identifying an epilepsy syndrome is useful as it helps determine the underlying causes as well as what anti-seizure medication should be tried.

The ability to categorize a case of epilepsy into a specific syndrome occurs more often with children since the onset of seizures is commonly early. Less serious examples are benign rolandic epilepsy (2.8 per 100,000), childhood absence epilepsy (0.8 per 100,000) and juvenile myoclonic epilepsy (0.7 per 100,000). Severe syndromes with diffuse brain dysfunction caused, at least partly, by some aspect of epilepsy, are also referred to as epileptic encephalopathies. These are associated with frequent seizures that are resistant to treatment and severe cognitive dysfunction, for instance Lennox-Gastaut syndrome and West syndrome.

Epilepsies with onset in childhood are a complex group of diseases with a variety of causes and characteristics. Some people have no obvious underlying neurological problems or metabolic disturbances. They may be associated with variable degrees of intellectual disability, elements of autism, other mental disorders, and motor difficulties. Others have underlying inherited metabolic diseases, chromosomal abnormalities, specific eye, skin and nervous system features, or malformations of cortical development. Some of these epilepsies can be categorized into the traditional epilepsy syndromes. Furthermore, a variety of clinical syndromes exist of which the main feature is not epilepsy but which are associated with a higher risk of epilepsy. For instance between 1 and 10% of those with Down syndrome and 90% of those with Angelman syndrome have epilepsy.

In general, genetics is believed to play an important role in epilepsies by a number of mechanisms. Simple and complex modes of inheritance have been identified for some of them. However, extensive screening has failed to identify many single rare gene variants of large effect. In the epileptic encephalopathies, de novo mutagenesis appear to be an important mechanism. De novo means that a child is affected, but the parents do not have the mutation. De novo mutations occur in eggs and sperms or at a very early stage of embryonic development. In Dravet syndrome a single affected gene was identified.

Syndromes in which causes are not clearly identified are difficult to match with categories of the current classification of epilepsy. Categorization for these cases is made somewhat arbitrarily. The "idiopathic" (unknown cause) category of the 2011 classification includes syndromes in which the general clinical features and/or age specificity strongly point to a presumed genetic cause. Some childhood epilepsy syndromes are included in the unknown cause category in which the cause is presumed genetic, for instance benign rolandic epilepsy. Others are included in "symptomatic" despite a presumed genetic cause (in at least in some cases), for instance Lennox-Gastaut syndrome. Clinical syndromes in which epilepsy is not the main feature (e.g. Angelman syndrome) were categorized "symptomatic" but it was argued to include these within the category "idiopathic". Classification of epilepsies and particularly of epilepsy syndromes will change with advances in research.