Antisocial Personality Disorder – Defined and Explained

Antisocial Personality Disorder – Defined and Explained
Antisocial Personality Disorder – Defined and Explained

The term Antisocial Personality Disorder or ASPD for short, refers to a chronic mental condition involving a pattern of disregard for the rights of others including the violation of other’s rights. Deceit and manipulation are common features of this personality disorder.

Personality disorders refer to mental health conditions related to the way a person feels, thinks, perceives or relates to others. Antisocial personality disorder is a pretty difficult personality disorder as the behavior of people with this disorder might be irresponsible, manipulative, impulsive, reckless, and indifferent to other’s feelings. Most often this personality disorder will lead to criminal behavior.

In DSM 5 it is included in cluster B, called emotional, dramatic and erratic cluster. The disorders in cluster B are characterized by problems with emotional regulation and impulse control.

This cluster also includes disorders such as Histrionic Personality Disorder, Narcissistic Personality Disorder, Borderline Personality Disorder and of course Antisocial Personality Disorder.

In ICD 10 it appears under the name of Dissocial Personality Disorder. The criteria are similar in both manuals (ICD – 10 and DSM – V) but not identical.

In both manuals it is mentioned that the antisocial personality disorder was often referred to as sociopathy or psychopathy and it might include psychopathy and sociopathy. But the two terms are not recognized or used by professionals to label diagnostics of antisocial personality disorder.

The diagnostic criteria for antisocial personality disorder were based on the work of Hervey Cleckley on psychopathy. Anyway there were critics who argued that as long as the criteria are not exactly the same, the antisocial personality disorder and psychopathy cannot be treated the same way.

Psychopathy is described as a personality disorder defined by traits that includes diminished ability for remorse, antisocial behavior and poor behavioral controls.

Most often psychopathy traits are measured using PCL-R (Psychopathy Checklist Revised), developed by Canadian researcher Robert D. Hare. Psychopathy diagnosis appears nowhere in the DSM or ICD though sometimes distinctions between the antisocial personality disorder and psychopathy or sociopathy are stated.

The spectrum of severity of antisocial personality disorder might range from a mild form that includes occasional bad behavior to a more severe version where the people with the disorder commit serious crimes and break the law repeatedly.

Robert Hare insists that his PCL-R is better than ASPD when it comes to predicting future violence and criminality though ASPD diagnosis covers twice or even three times more prisoners than psychopathy diagnosis.

In DSM – V psychopathy was proposed as an alternative model of ASPD, called Alternative DSM – 5 Model for Personality disorder. It is a diagnosis of ASPD with psychopathic features and it is described as the lack of fear or anxiety and bold interpersonal style that could mask fraudulence.

Five Subtypes Of ASPD Were Proposed By Theodore Millon:

  • Nomadic – with avoidant and schizoid features.
  • Malevolent – with paranoid and sadistic features.
  • Covetous – feels deprived and denied and finds more pleasure in taking than having.
  • Risk-taking – with histrionic features.
  • Reputation defending – with narcissistic features.
  • Male are more likely to be diagnosed with ASPD than women and people with ASPD are at higher risk of a violent death.

Also There Are Few Disorders That Are Very Likely To Coexist With ASPD Including:

  • Anxiety disorders.
  • Impulse control disorders.
  • ADHD.
  • Depressive disorders.
  • Borderline personality disorder.
  • Narcissistic personality disorder.
  • Somatization disorder.
  • Substance related disorders.
  • Sadistic personality disorder.
  • Histrionic personality disorder.

The factors that might cause ASPD include imbalance between levels of testosterone, cortisol and serotonin. The three substances aforementioned seem to be important regulators of social aggression.

Other factors might include head injury, limbic neural maldevelopment, home and social environment or even cultural influences. Also there are scientists who think the ASPD might be inherited.

The ASPD should be diagnosed only by a trained psychiatrist and in order to understand this disorder people should seek the specialist help of a psychiatrist.

The treatment for ASPD is really difficult as the patient lacks remorse and the symptoms include deceitfulness. The most common treatment for ASPD are psychotherapy and cognitive behavioral therapy.

Cranial Arteritis – What It is and Diagnosis

Cranial Arteritis – What It is and Diagnosis
Cranial Arteritis – What It is and Diagnosis

Cranial arteritis is a term used rarely. The disease is most often called GCA (Giant-Cell Arteritis) or temporal arteritis. The term refers to an inflammation of the blood vessels in the head especially the branches of the external carotid artery.

Basically it’s a form of vasculitis that usually causes inflammation of the small vessels that supply the larger arteries. Arteries of the head and neck are affected most often including the axillary arteries, the thoracic aorta and the vertebral arteries.

The occlusion of the ophthalmic artery is the most serious complication and it can cause blindness and irreversible ischema if it is not treated immediately. The exact cause of the condition is still unknown. Scientists believe it is due to a faulty immune response. The use of high large amounts of antibiotics and severe infections were linked to the disorder. The condition may spread following polymyalgia rheumatic. The GCA is rare in African descendants and almost always appears in people over age 50.

The Signs and Symptoms Might Include:

Headache,Fever, bruits, tongue and jaw claudication, tenderness and sensitivity to the scalp, acute tinnitus, reduced visual acuity and diplopia.

In 50% of the case the disorder coexists with polymyalgia rheumatica characterized by stiffness and pain in the muscles.

For a correct diagnosis the doctor will examine the head of the patient and if the patient has GCA there will be thick tender artery on one side of the head, most often over the temples. Also the scalp usually is sensitive. Then blood tests are used and might include hematocrit or hemoglobin, C-creative protein, liver function test and sedimentation rate. Because blood tests alone won’t be enough for a diagnosis a tissues sample from the artery involved will be necessary too. Other tests might include MRI, duplex ultrasound and PET scan.

Receiving the treatment immediately is crucial to preventing severe complications and problems like stroke or blindness. Corticosteroids are administered orally, most often even before biopsy. Often aspirin is recommended. Usually there is improvement a few days after the treatment start. But the treatment might require medicine to be taken for 1 to 2 years. And the doses of corticosteroids will be cut back really slow.

Because of the long-term treatment with corticosteroids the bones might get frailer and the chance of fracture will increase. Therefore taking calcium and D vitamin supplements is often recommended. Also patients should quit smoking and the bones will be examined with a DEXA scan or a BMD (bone mineral density) test. Other medicine that suppresses the immune system might also be used.

After a long treatment of 1 to 2 years long, most of the people recover completely. Unfortunately the condition might return later. Aneurysm or other damage in the blood vessels might also occur and in the future that damage could cause a stroke.

Any symptom of temporal arteritis or throbbing ache should be taken seriously as a warning sign and a specialist should be consulted immediately or else permanent visual impairment might occur. The specialist assistance of a neurologist could help the patient understand the condition better.

So far there is no method of preventing this condition.

Encephalotrigeminal Angiomatosis

Encephalotrigeminal Angiomatosis

Encephalotrigeminal Angiomatosis which is also known as Sturge-Weber syndrome is an innate disorder that is characterized by a distinct vascular birthmark as well as neurological anomalies. This condition might be inclusive of eye and other internal organ anomalies.

Signs and Symptoms

Encephalotrigeminal Angiomatosis is commonly diagnosed clinically. The clinical diagnose is typically based on the central nervous system, cutaneous, and other ocular abnormalities related to the condition. Some of the neurologic symptoms include;

  • Learning problems
  • Mental retardation
  • Developmental delay
  • Attention deficit or hyperactivity disorder

Physical signs associated with Encephalotrigeminal Angiomatosis include;

  • Ocular manifestations
  • Macrocephaly
  • Soft-tissue hypertrophy
  • Visual loss
  • Hemiparesis
  • Hemianopsia
  • PWS

Involvement of ocular in Encephalotrigeminal Angiomatosis might include signs such as;

  • Glaucoma
  • Hemangiomalike or apparent changes on the eyelids
  • Buphthalmos

Causes of Encephalotrigeminal Angiomatosis

The condition occurs sporadically. It’s generally not genetic and therefore can’t be passed to children by the parents. It usually starts quite early during pregnancy as the infant is developing inside the womb. Basically at 6 to 9 weeks during pregnancy the body tissues responsible for brain and skin formation are closely associated.

Experts suggest that the blood vessels network keeps developing instead of unraveling, resulting in formation of another blood vessel layer on the brain surface.

How common is Encephalotrigeminal Angiomatosis?

It is exactly not known how many individuals are affected by this condition but it’s only known to be a rare condition. The condition affects both girls and boys alike. Kids with the characteristic ‘port wine stain’ appearing on the forehead or either side of the scalp are quite likely to be having this condition.

Encephalotrigeminal Angiomatosis

Diagnosing Encephalotrigeminal Angiomatosis

If a child’s scalp or forehead has the port wine stain, they will need a pediatrician to check him or her. MRI scans including a gadolinium are used to determine a diagnosis. It’s basically similar to a normal MRI scan just that the child will have to be injected with gadolinium beforehand. A gadolinium injection ensures the blood vessels get displayed better during the scan. If the diagnosis is determined then a pediatrician and the pediatric neurologist can work together to work out the problem.

Other Manifestations

Glaucoma or high pressure around the eyes is one of the conditions that are apparent at birth time or show up later. The occurrence of the glaucoma in persons with the Encephalotrigeminal Angiomatosis is said to be about 40% and 70% in choroidal lesions. Glaucoma is normally limited to the eye covered by the stain. Also eye enlargement (buphthalmos) is also a common occurrence for the stain affected eye. Numerous other bodily organs are less affected by the condition.


Treatment by way of laser is employed to get rid of and/or lighten the birthmarks for children as little as a month old. By use of anti-convulsants, seizures can easily be controlled. Also a brain surgery as well as VNS implants can be employed to assist in seizure management. Oral medications or eye drops can be used to help manage glaucoma. Should all the oral and topical administered medications fail to be effective, then the only other option would certainly be surgery.

Chorea Athetosis and Hemiballismus – Details, Causes

Chorea Athetosis and Hemiballismus – Details, Causes

There three disorders are very similar and they belong to a group of disorders called the hyperkinectic disorders that also include dyskinesia and dystonia. They describe abnormal involuntary non-stereotypical movement disorders. As they are pretty similar it is very important to differentiate them and for a better understanding of these conditions you might need the specialist assistance of a neurologist.

Chorea Athetosis

From the very beginning it’s important to understand that all three disorders involve abnormal involuntary non-stereotypical movement. The difference consists in the muscles affected, speed and style.

Chorea involves rapid, non-stereotypical,jerky, involuntary, repetitive, dance-like movements. The moves involve the distal muscle group more than the proximal.

Unlike chorea, athetosis is a slow non-stereotypical, repetitive, involuntary, writing movement that usually affects the upper limbs.

Ballismus is also a rapid non-stereotypical, involuntary, repetitive and relatively more violent move that affects the proximal muscle group more than the distal.

Many times athetosis and chorea occur together and that is called choreoathetosis.

The involuntary movements might merge into semipurposeful or purposeful acts that could mask them.

Chorea is a progressive neurological disorder that is caused most often by Huntington’s disease. Rheumatic fever can also cause what is called the Sydenham’s chorea. Rarely, it might appear during pregnancy. The type of chorea that appears during pregnancy is called chorea gravidarum. Other causes might involve Wilson’s disease, neuroacanthocytosis and Transmissible spongiform encephalopathies.

As there is no cure for the disease there is no standard course of treatment and is symptomatic. The treatment depends on the type of chorea and there are a few medicines that can control it.

In the case of Huntington’s-related chorea the supportive treatment uses Tetrabenazine. In the case of Sydenham’s chorea the treatment involves valproic acid, Haloperidol and carbamazepine. If Wilson’s disease is causing chorea the treatment will involve chlorpromazine, haloperidol and pimozide.

The athetosis is usually caused by Huntington’s disease or marbling. In rare cases it is caused by trauma or stroke. Sometimes it might be caused by complications at birth especially neonatal jaundice and intranatal asphyxia. There are meny treatments used to help people with athetosis and most often drugs are used but sometimes surgery might be required.

The most common drugs used to treat athetosis are haloperidol, tetrabenazine, congentin, thiopropazate, artane and diazepam. The surgery might involve cutting a part of the posterior spinal roots or the removal of a part of the cerebral motor cortex. Surgery can produce immediate effects and is very beneficial on short term but they are not lasting too long. Retraining movements for the affected person is also a part of the treatment of athetosis.

Hemiballismus is a very rare disorder which can result from many various causes such as amyotrophic lateral sclerosis, stroke, vascular malformations, tuberculomas, traumatic brain injury, nonketotic hyperglycemia, neoplasms, demyelinating plaques and complications from HIV infections.

The treatment focuses on anything that causes the manifestations and symptoms of the disorder and it might include dopamine blockers, ITB therapy, botulinum injections, anticonvulsants, antipsychotics, tetrabenazine or functional neurosurgery.

Because the disorder is very rare the researchers and specialists know very little about it and there many unanswered questions. For an instance they try to explain the differences between this disorder in animals and humans. Also they try to understand why certain treatments help people with hemiballismus when they are very likely to do more harm.

Here Is A Clean Example Of A Girl Suffering From Chorea Athetosis and Hemiballismus