Clinical vampirism, more commonly called Renfield's syndrome or Renfield syndrome, is an obsession with drinking blood. The earliest formal presentation of clinical vampirism to appear in the psychiatric literature, with the psychoanalytic interpretation of two cases, was contributed by Richard L. Vanden Bergh and John F. Kelley in 1964. As the authors point out, brief and sporadic reports of blood-drinking behaviors associated with sexual pleasure have appeared in the psychiatric literature at least since 1892 with the work of Austrian forensic psychiatrist Richard von Krafft-Ebing. Many medical publications concerning clinical vampirism can be found in the literature of forensic psychiatry, with the unusual behavior reported as one of many aspects of extraordinary violent crimes. The behavior has never gained official recognition by the psychiatric profession and is not found in any edition of the "International Classification of Diseases" or the "Diagnostic and Statistical Manual of Mental Disorders".

Involutional melancholia is classically treated with antidepressants and mood elevators.

Electroconvulsive therapy may also be used. Mid-century, there was a consensus that the technique indeed 'yields the best results in the long-lasting depressions of the change of life, the so-called "involutional melancholias", which before this form of treatment was introduced often required years of hospitalization'. The 21st century also records 'an excellent and rapid clinical response found in melancholia of recent onset...in older rather than younger patients' with ECT

"Species dysphoria" is informally used mainly in psychological literature to compare the experiences of some individuals to those in the transgender community. Otherkin and therian communities have also used it to describe their experiences.

In a 2008 study by Gerbasi "et al.", 46% of people surveyed who identified as being in the furry fandom, (usually defined as a person who enjoys anthropomorphic animals, occasionally to an almost obsessive degree), answered "yes" to the question "Do you consider yourself to be less than 100% human?" and 41% answered "yes" to the question "If you could become 0% human, would you?" Questions that Gerbasi states as being deliberately designed to draw parallels with gender dysphoria, specifying "a persistent feeling of discomfort" about the human body and the feeling that the person was the "non-human species trapped in a human body", were answered "yes" by 24% and 29% of respondents, respectively. Likewise, these studies support the fact that the therianthropic, otherkin and furry communities are very similar in nature and are often interconnected.

As described by those who experience it, species dysphoria may include sensations of supernumerary phantom limbs associated with the species, such as phantom wings or claws. Species dysphoria involves feelings of being an animal or other creatures "trapped in" a human body and so, is considered different from the traditional definition of clinical lycanthropy, in which the patient believes they have actually been transformed into an animal or have the ability to physically shapeshift. However, some cases that have been labeled as "clinical lycanthropy" actually seem to be cases of species dysphoria, involving persons who have no delusion of transformation but instead have feelings of being in some way a non-human animal, while still acknowledging they possess a human form. Keck "et al." propose a redefinition for clinical lycanthropy that covers species dysphoric behaviours observed in several patients, including verbal reports, "during intervals of lucidity or retrospectively, that he or she was a particular animal" and behaving "in the manner of a particular animal, i.e. howling, growling, crawling on all fours". Keck "et al." describe one patient as a depressed individual who "had always suspected he was a cat" and "laments his lack of fur, stripes and a tail". Except for the persistent feeling of being feline, the patient's "thought processes and perception" were "usually logical".

Species dysphoria is the experience of dysphoria, sometimes including clinical lycanthropy (delusion or hallucination of one's self as an animal) and dysmorphia (excessive concern over one's body image), associated with the feeling that one's body is of the wrong species. Earls and Lalumière (2009) describe it as "the sense of being in the wrong (species) body... a desire to be an animal". Outside of psychological literature, the term is common within the otherkin and therian communities. The phenomenon is sometimes experienced in the context of sexual arousal to the image of one's self as an animal.

Affected individuals believe that they are in the process of transforming into an animal or have already transformed into an animal. It has been associated with the altered states of mind that accompany psychosis (the that typically involves delusions and hallucinations) with the transformation only seeming to happen in the mind and behavior of the affected person.

A study on lycanthropy from the McLean Hospital reported on a series of cases and proposed some diagnostic criteria by which lycanthropy could be recognised:

- A patient reports in a moment of lucidity or reminiscence that they sometimes feel as an animal or have felt like one.

- A patient behaves in a manner that resembles animal behavior, for example howling, growling, or crawling.

According to this criteria, either a delusional belief in current or past transformation or behavior that suggests a person thinks of themselves as transformed is considered evidence of clinical lycanthropy. The authors note that, although the condition seems to be an expression of psychosis, there is no specific diagnosis of mental or neurological illness associated with its behavioral consequences.

DSM-IV Criteria

Clinical Lycanthropy is thought to be a cultural manifestation of schizophrenia due to the first 4 symptomatic criteria. The first criteria are delusions, and this fits clinical lycanthropy because a person believing that he or she turns into an animal is a delusion. The second symptom is hallucination, and people with clinical lycanthropy have vivid hallucinations of being an animal, and having traits that animal has, whether it be claws, fur, fangs, or whatever that particular animal has. The next symptom is disorganized speech, from a certain human, cultural perspective. The people who have the diagnosis of clinical lycanthropy often emit the sounds of the animal which they believe they become. So, if a person believes that he or she is a werewolf, they may begin to howl under the moon or sometimes even in the daylight. The last symptom that matches schizophrenia is grossly disorganized behavior. This is appropriate because individuals with clinical lycanthropy often act like the animal they believe they have become, including living outside and changing their diet.

It also seems that lycanthropy is not specific to an experience of human-to-wolf transformation; a wide variety of creatures have been reported as part of the shape-shifting experience. A review of the medical literature from early 2004 lists over thirty published cases of lycanthropy, only the minority of which have wolf or dog themes. Canines are certainly not uncommon, although the experience of being transformed into a hyena, cat, horse, bird or tiger has been reported on more than one occasion. Transformation into frogs, and even bees, has been reported in some instances. In Japan, transformation into foxes and dogs was usual (, ). A 1989 case study described how one individual reported a serial transformation, experiencing a change from human to dog, to horse, and then finally cat, before returning to the reality of human existence after treatment. There are also reports of people who experienced transformation into an animal only listed as "unspecified".

There is a case study of a psychiatric patient who had both clinical lycanthropy and Cotard delusion. The term "ophidianthropy" refers to the delusion that one has been transformed into a snake. Two case studies have been reported.

Clinical lycanthropy is a rare condition and is largely considered to be an idiosyncratic expression of a psychotic episode caused by another condition such as schizophrenia, bipolar disorder or clinical depression.

However, there are suggestions that certain neurological conditions and cultural influences may result in the expression of the human-animal transformation theme that defines the condition.

The syndrome (also Renfield syndrome) is named after Dracula's human zoophagous follower, R. M. Renfield, in the 1897 novel by Bram Stoker. According to an interview conducted by psychology professor Katherine Ramsland with clinical psychologist Richard Noll, who coined the eponymous term in a 1992 book, he invented the term and its purported diagnostic criteria as a whimsical parody of the "new DSM-speak" of the psychiatry of the 1980s. In a public lecture hosted by Penn State University's Institute for the Arts and Humanities on 7 October 2013, Noll traced the 20-year trajectory of his unintentionally created "monster" from the moment of its creation as a parody of DSM mental disorders to the cultural popularity of Renfield's syndrome today.

After Noll's book appeared in 1992 clinical vampirism has usually been referred to as Renfield's syndrome. In an NBC pre-Halloween special hosted by actor Peter Graves entitled "The Unexplained: Witches, Werewolves and Vampires" that aired on 23 October 1994 (and is available on YouTube, with the 34:11 mark beginning the segment), pages from Noll's book were shown on camera as Canadian psychologist Leonard George summarized Renfield's syndrome for a wide television audience.

Characters suffering from Renfield's Syndrome have appeared on television. The first appeared in a 2005 episode of "" titled "Committed" (Season 5, Episode 21). It was also mentioned in 2009 in episode 7, season 5 of "Criminal Minds" entitled "The Performer".

In 2010 an 11-episode Canadian television series, "The Renfield Syndrome", was filmed in Vancouver, B.C., but does not seem to have been aired.

On 15 August 2012 Renfield's syndrome was the subject of a video segment on "The Huffington Post" by Cara Santa Maria which again relied heavily on Noll's work and a recent scholarly article on the (pseudo-)syndrome published in the "Journal of the History of the Neurosciences".

In addition to references to Renfield's syndrome in the psychiatric literature and mass media, the horror writer Chelsea Quinn Yarbro published a story entitled "Renfield's Syndrome" in July 2002, which was then reprinted in an anthology that appeared the following year. It is also the title of a novel by J.A. Saare.

The twenty-year evolution of a farcical 3-page book section that shot through the mass media and then—uncritically—into the pages of a peer-reviewed scholarly journal should serve as a cautionary tale about the purported validity of other "mental disorders." Philosopher of science Ian Hacking refers to this process as "making up people" and critiques medical and psychiatric elites for the untoward effects of their "dynamic nominalism" on individual lives. Such arbitrary categories create new natural "kinds" of people (e.g., perverts, multiple personalities and so on) that serve larger political, cultural and moral purposes and change with historical contingencies.

According to the case history reports in the older psychiatric literature that formed the basis of Noll's parody, the condition starts with a key event in childhood that causes the experience of blood injury or the ingestion of blood to be exciting. After puberty, the excitement is experienced as sexual arousal. Throughout adolescence and adulthood, blood, its presence, and its consumption can also stimulate a sense of power and control. Noll speculated that Renfield's syndrome begins with autovampirism and then progresses to the consumption of the blood of other creatures.

The usefulness of this diagnostic label remains in question. Very few cases of the syndrome have been described, and the published reports that do exist refer to what has been proposed as Renfield's syndrome through the use of official psychiatric diagnostic categories such as schizophrenia or as a variety of paraphilia.

The medical management of FXTAS aims to reduce the level of disability and minimize symptoms. Presently, there are many gaps in the research on the management of FXTAS, as the disorder was first described in the literature in 2001. There is no treatment modality aimed at reversing the pathogenesis of FXTAS. However, there are a variety of drug therapies that are being utilized in the management of FXTAS symptoms, although there is a lack of randomized control trials assessing the efficacy these therapies and support is limited to anecdotal evidence. Therefore, many of the treatments are based on what has been helpful in disorders with similar clinical presentations.

There is no cure for FXTAS. Current treatment includes medications for alleviating symptoms of tremor, ataxia, mood changes, anxiety, cognitive decline, dementia, neuropathic pain, or fibromyalgia. Neurological rehabilitation has not been studied for patients with FXTAS but should also be considered as a possible form of therapy. Additionally, occupational and physical therapy may help to improve performance of functional tasks.

Involutional melancholy's 'course was chronic, with agitation, depersonalization and delusions of bodily change and guilt' featuring strongly, but 'without manic features'. Symptoms of fear are also considered to occur, as well as despondency and hypochondriacal delusions. The late onset of the disorder was matched with a prolonged course with poor prognosis and/or deterioration, in the absence of treatment.

there are no USFDA-approved medications for the treatment of mild cognitive impairment. Moreover, as of January 2018, there is no high-quality evidence that supports the efficacy of any pharmaceutical drugs or dietary supplements for improving cognitive symptoms in individuals with mild cognitive impairment. A moderate amount of high-quality evidence supports the efficacy of regular physical exercise for improving cognitive symptoms in individuals with MCI. The clinical trials that established the efficacy of exercise therapy for MCI involved twice weekly exercise over a period of six months. A small amount of high-quality evidence supports the efficacy of cognitive training for improving some measures of cognitive function in individuals with mild cognitive impairment. Due to the heterogeneity among studies which assessed the effect of cognitive training in individuals with MCI, there are no particular cognitive training interventions that have been found to provide greater symptomatic benefits for MCI relative to other forms of cognitive training.

The American Academy of Neurology's (AAN) clinical practice guideline on mild cognitive impairment from January 2018 stated that clinicians "should" identify modifiable risk factors in individuals with MCI, assess functional impairments, provide treatment for any behavioral or neuropsychiatric symptoms, and monitor the individual's cognitive status over time. It also stated that medications which cause cognitive impairment "should" be discontinued or avoided if possible. Due to the lack of evidence supporting the efficacy of cholinesterase inhibitors in individuals with MCI, the AAN guideline stated that clinicians who choose to prescribe them for the treatment of MCI "must" inform patients about the lack of evidence supporting this therapy. The guideline also indicated that clinicians "should" recommend that individuals with MCI engage in regular physical exercise for cognitive symptomatic benefits; clinicians "may" also recommend cognitive training, which appears to provide some symptomatic benefit in certain cognitive measures.

As MCI may represent a prodromal state to clinical Alzheimer's disease, treatments proposed for Alzheimer's disease, such as antioxidants and cholinesterase inhibitors, could potentially be useful; however, there is no evidence to support the efficacy of cholinesterase inhibitors for the treatment of mild cognitive impairment. Two drugs used to treat Alzheimer's disease have been assessed for their ability to treat MCI or prevent progression to full Alzheimer's disease. Rivastigmine failed to stop or slow progression to Alzheimer's disease or to improve cognitive function for individuals with mild cognitive impairment; donepezil showed only minor, short-term benefits and was associated with significant side effects.

In a two-year randomized trial of 168 people with MCI given either high-dose vitamins or placebo, vitamins cut the rate of brain shrinkage by up to half. The vitamins were the three B vitamins folic acid, vitamin B6, and vitamin B12, which inhibit production of the amino acid homocysteine. High blood levels of homocysteine are associated with increased risk of cognitive decline, dementia, and cardiovascular disease. A single study from 2012 showed a possible connection between macronutrient intake and development of MCI. It is also suggested that a dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of MCI or dementia in elderly persons

Experimental non-pharmacological treatments for MCI include transcranial magnetic stimulation and transcranial direct current stimulation; the efficacy of these interventions for the treatment of MCI has not yet been established.

Somatic manifestations of MD are distinguished by an extreme diversity and include headaches, back pain, abdominal pain etc. Pathological behaviour masking depression may take the form of compulsive gambling, compulsive work, changes in arousal or orgasmic function, decreased libido or, on the contrary, impulsive sexual behaviour, alcoholism, drug addiction and more.

Masked depression (MD) was a proposed form of atypical depression in which somatic symptoms or behavioural disturbances dominate the clinical picture and disguise the underlying affective disorder. The concept is not currently supported by the mental health profession.

While there is no cure for HPS, treatment for chronic hemorrhages associated with the disorder includes therapy with vitamin E and the antidiuretic dDAVP.

Since interleukin 1β plays a central role in the pathogenesis of the disease, therapy typically targets this cytokine in the form of monoclonal antibodies (such as canakinumab), binding proteins/traps (such as rilonacept), or interleukin 1 receptor antagonists (such as anakinra). These therapies are generally effective in alleviating symptoms and substantially reducing levels of inflammatory indices. Case reports suggest that thalidomide and the anti-IL-6 receptor antibody tocilizumab may also be effective.

A preoperative pulmonology consultation is needed. The anesthesia team should

be aware that patients may have postoperative pulmonary complications as part

of the syndrome.

Preoperative hematology consultation is advisable prior to elective ocular

surgeries. Since patients with the syndrome have bleeding tendencies,

intraoperative, perioperative, and postoperative hemorrhages should be

prevented and treated. If platelet aggregation improves with desmopressin, it

may be administered in the preoperative period. However, sometimes

plasmapheresis is needed in the perioperative period.

Ophthalmologists should try to avoid retrobulbar blocks in patients with the

syndrome. Whenever possible, patients with HPS may benefit from general

endotracheal anesthesia. Phacoemulsification may help prevent intraoperative

and postoperative bleeding in patients with the syndrome. Prolonged bleeding

has been reported following strabismus surgery in patients with the syndrome.

Behavioral treatment can be effective in some cases. Sedative hypnotics may also help relieve the symptoms. Additionally, education about normal patterns of the sleep-wake cycle may alleviate anxiety in some patients. For patients with severe depression resulting from the fear of having insomnia, electroconvulsive therapy appears to be a safe and effective treatment.

In terms of beta-mannosidosis treatment there is none currently, individuals that exhibit muscle weakness or seizures are treated based on the symptoms(since there's no cure)

Treatment of opioid tolerance and Opioid-Induced Hyperalgesia (OIH) differs but it may be difficult to differentiate these two conditions in a clinical setting where most pain assessments are done through simple scale scores. The treatment for OIH may be challenging because an inadequate number of quality studies exists possibly due to the complexity in diagnosis of OIH and challenges in working with patients on chronic opioids. Currently there is no single best treatment method for OIH and clinicians are advised to choose an appropriate therapy based on the unique clinical scenario and history of each patient.

One general treatment option is to reduce or discontinue the dose of opioid to see if OIH is improved. Opioid sparing or opioid switching, which is replacing the current opioid with another pharmacological agent such as morphine or methadone, has been reported to be effective in some studies but this may also increase the sensitivity to pain according to some case reports. Ketamine, a NMDA antagonist, has been shown to prevent the extended use of opioid in post-operative hyperalgesia when it is infused in a small amount perioperatively along with the opioid but there are also studies that show ketamine being ineffective in modulating hyperalgesia. Addition of the NSAID, especially some COX-2 inhibitors, or acetaminophen is also suggested as a possible treatment option.

The condition may worsen as a result of persistent attempts to treat the symptoms through conventional methods of dealing with insomnia. The prescription of hypnotics or stimulants may lead to drug dependency as a complication.

Nonetheless, chronic SSM may increase risk for depression, anxiety, and substance abuse. It has also been noted that patients with this condition may sometimes opt to take medications over other treatments "for the wrong reasons (e.g. because of euphoriant properties)."

Gianotti-Crosti disease is a harmless and self-limiting condition, so no treatment may be required. Treatment is mainly focused on controlling itching, symptomatic relief and to avoid any further complications. For symptomatic relief from itching, oral antihistamines or any soothing lotions like calamine lotion or zinc oxide may be used. If there are any associated conditions like streptococcal infections, antibiotics may be required.

First-line treatment for CIDP is currently intravenous immunoglobulin (IVIG) and other treatments include corticosteroids (e.g. prednisone), and plasmapheresis (plasma exchange) which may be prescribed alone or in combination with an immunosuppressant drug. Recent controlled studies show subcutaneous immunoglobin (SCIG) appears to be as effective for CIDP treatment as IVIG in most patients, and with fewer systemic side effects.

IVIG and plasmapheresis have proven benefit in randomized, double-blind, placebo-controlled trials. Despite less definitive published evidence of efficacy, corticosteroids are considered standard therapies because of their long history of use and cost effectiveness. IVIG is probably the first-line CIDP treatment, but is extremely expensive. For example, in the U.S., a single 65 g dose of Gamunex brand in 2010 might be billed at the rate of $8,000 just for the immunoglobulin—not including other charges such as nurse administration. Gamunex brand IVIG is the only U.S. FDA approved treatment for CIDP, as in 2008 Talecris, the maker of Gamunex, received orphan drug status for this drug for the treatment of CIDP.

Immunosuppressive drugs are often of the cytotoxic (chemotherapy) class, including rituximab (Rituxan) which targets B cells, and cyclophosphamide, a drug which reduces the function of the immune system. Ciclosporin has also been used in CIDP but with less frequency as it is a newer approach. Ciclosporin is thought to bind to immunocompetent lymphocytes, especially T-lymphocytes.

Non-cytotoxic immunosuppressive treatments usually include the anti-rejection transplant drugs azathioprine (Imuran/Azoran) and mycophenolate mofetil (Cellcept). In the U.S., these drugs are used as "off-label" treatments for CIDP, meaning that their use here is accepted by the FDA, but that CIDP treatment is not explicitly indicated or approved in the drug literature. Before azathioprine is used, the patient should first have a blood test that ensures that azathioprine can safely be used.

Anti-thymocyte globulin (ATG), an immunosuppressive agent that selectively destroys T lymphocytes is being studied for use in CIDP. Anti-thymocyte globulin is the gamma globulin fraction of antiserum from animals that have been immunized against human thymocytes. It is a polyclonal antibody.

Although chemotherapeutic and immunosuppressive agents have shown to be effective in treating CIDP, significant evidence is lacking, mostly due to the heterogeneous nature of the disease in the patient population in addition to the lack of controlled trials.

A review of several treatments found that azathioprine, interferon alpha and methotrexate were not effective. Cyclophosphamide and rituximab seem to have some response. Mycophenolate mofetil may be of use in milder cases. Immunoglobulin and steroids are the first line choices for treatment. Rarely bone marrow transplantation has been performed.

Physical therapy and occupational therapy may improve muscle strength, activities of daily living, mobility, and minimize the shrinkage of muscles and tendons and distortions of the joints.

The main treatment for acral erythema is discontinuation of the offending drug, and symptomatic treatment to provide analgesia, lessen edema, and prevent superinfection. However, the treatment for the underlying cancer of the patient must not be neglected. Often, the discontinued drug can be substituted with another cancer drug or cancer treatment.

Symptomatic treatment can include wound care, elevation, and pain medication. Corticosteroids and pyridoxine have also been used to relieve symptoms. Other studies do not support the conclusion.

A number of additional remedies are listed in recent medical literature. Among them henna and 10% uridine ointment which went through clinical trial.

Heterogeneous medical condition in medicine are those medical conditions which have several etiologies, like hepatitis or diabetes. Medical conditions are normally defined pathologically (liver inflammation) or clinically (excessive urination) and not etiologically, and therefore it is normal to have more than one cause for them. The word is used as an opposition to homogeneous, meaning that given a group of patients, the disease is the same for all of them.

When a condition is heterogeneous, it is normally divided in endotypes.

Infusions of immune globulin can reduce the frequency of bacterial infections, and G-CSF or GM-CSF therapy improves blood neutrophil counts.

As WHIM syndrome is a molecular disease arising from gain-of-function mutations in CXCR4, preclinical studies identified plerixafor, a specific CXCR4 antagonist, as a potential mechanism-based therapeutic for the disease. Two subsequent clinical trials involving a handful of patients with WHIM syndrome demonstrated that plerixafor could increase white blood cell counts and continues to be a promising targeted therapy.

A woman with spontaneous remission of her WHIM syndrome due to Chromothripsis in one of her blood stem cells has been identified.

In support of these studies, a 2014 phase I clinical trial treated 3 patients diagnosed with WHIM syndrome with plerixafor twice a day for 6 months. All three patients presented with multiple reoccurring infections before treatment and all had an increase in their white blood cell count post treatment. One patient (P3) had a decrease in his infections by 40% while the remaining 2 patients (P1 and P2) had no infections throughout the entirety of the treatment. Plerixafor may also proof to have anti-human papillomavirus (HPV) properties as all patients experienced a shrinkage or complete disappearance of their warts. While this treatment shows promise in treating neutropenia (decreased white blood cells), this trial showed no increase of immune globulins in the body. A phase III clinical trial has been approved to compare the infection prevention ability of plerixafor versus the current treatment of G-CSF in patients with WHIM.

There is currently no therapy or cure for MLD in late infantile patients displaying symptoms, or for juvenile and adult onset with advanced symptoms. These patients typically receive clinical treatment focused on pain and symptom management.

Pre-symptomatic late infantile MLD patients, as well as those with juvenile or adult MLD that are either presymptomatic or displaying mild symptoms, can consider bone marrow transplantation (including stem cell transplantation), which may slow down progression of the disease in the central nervous system. However, results in the peripheral nervous system have been less dramatic, and the long-term results of these therapies have been mixed. Recent success has involved stem cells being taken from the bone marrow of children with the disorder and infecting the cells with a retro-virus, replacing the stem cells' mutated gene with the repaired gene before re-injecting it back into the patient where they multiplied. The children by the age of five were all in good condition and going to kindergarten when normally by this age, children with the disease can not even speak.

Several therapy options are currently being investigated using clinical trials primarily in late infantile patients. These therapies include gene therapy, enzyme replacement therapy (ERT), substrate reduction therapy (SRT), and potentially enzyme enhancement therapy (EET).

A team of international researchers and foundations gathered in 2008 to form an international MLD Registry to create and manage a shared repository of knowledge, including the natural history of MLD. This consortium consisted of scientific, academic and industry resources. This registry never became operational.