Bipolar Affective Disorder

Bipolar disorder or bipolar affective disorder, historically known as manic-depressive disorder, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.

Bipolar disorder, or manic-depressive illness (MDI), is one of the most common, severe, and persistent mental illnesses. Bipolar disorder is a serious lifelong struggle and challenge. It is also useful to note that other mental health disorders and general medical conditions are more prevalent in patients with bipolar disorders.

Bipolar disorder is characterized by periods of deep, prolonged, and profound depression that alternate with periods of an excessively elevated or irritable mood known as mania. The symptoms of mania include a decreased need for sleep, pressured speech, increased libido, reckless behavior without regard for consequences, grandiosity, and severe thought disturbances, which may or may not include psychosis. Between these highs and lows, patients usually experience periods of higher functionality and can lead a productive life.

Etiology
A number of factors contribute to bipolar disorder, including genetic, biochemical, psychodynamic, and environmental factors. Genetic factors contribute substantially to the likelihood of developing bipolar disorder, and environmental factors are also implicated.

First-degree relatives of people with BPI are approximately 7 times more likely to develop BPI than the general population.

Multiple biochemical pathways likely contribute to bipolar disorder, which is why detecting one particular abnormality is difficult.

In some instances, the cycle may be directly linked to external stresses or the external pressures may serve to exacerbate some underlying genetic or biochemical predisposition.

Pregnancy is a particular stress for women with a manic-depressive illness history and increases the possibility of postpartum psychosis.

Parkinson’s Disease

Parkinson disease is recognized as one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years.

Parkinson’s disease (also known as Parkinson disease, Parkinson’s, idiopathic parkinsonism, primary parkinsonism, PD, or paralysis agitans) is a degenerative disorder of the central nervous system. The motor symptoms of Parkinson’s disease result from the death of dopamine generating cells in the substantia nigra, a region of the midbrain.

The classic motor features of Parkinson disease typically start insidiously and emerge slowly over weeks or months, with tremor being the most common initial symptom. The 3 cardinal signs of Parkinson disease are resting tremor, rigidity, and bradykinesia.

Pathology
No specific, standard criteria exist for the neuropathologic diagnosis of Parkinson disease, as the specificity and sensitivity of its characteristic findings have not been clearly established. However, the following are the 2 major neuropathologic findings in Parkinson disease:
Loss of pigmented dopaminergic neurons of the substantia nigra pars compacta
The presence of Lewy bodies and Lewy neurites

The loss of dopamine neurons occurs most prominently in the ventral lateral substantia nigra. Approximately 60-80% of dopaminergic neurons are lost before the motor signs of Parkinson disease emerge.

Causes
Most people with Parkinson’s disease have idiopathic Parkinson’s disease (having no specific known cause). A small proportion of cases, however, can be attributed to known genetic factors. Other factors have been associated with the risk of developing PD, but no causal relationship has been proven.

Epidemiology
The incidence and prevalence of Parkinson disease increase with age, and the average age of onset is approximately 60 years. Onset in persons younger than 40 years is relatively uncommon. Parkinson disease is about 1.5 times more common in men than in women.

Clinical Presentation
Onset of motor signs in Parkinson disease is typically asymmetric, with the most common initial finding being an asymmetric resting tremor in an upper extremity. Over time, patients notice symptoms related to progressive bradykinesia, rigidity, and gait difficulty. The first affected arm may not swing fully when walking, and the foot on the same side may scrape the floor. Over time, axial posture becomes progressively flexed and strides become shorter.

Initial clinical symptoms in Parkinson disease include the following:

• Tremor
• A subtle decrease in dexterity; for example, a lack of coordination with activities such as playing golf or dressing (about 20% of patients first experience clumsiness in one hand)
• Decreased arm swing on the first-involved side
• Soft voice
• Decreased facial expression
• Sleep disturbances
• Decreased sense of smell
• Symptoms of autonomic dysfunction, including constipation, sweating abnormalities, sexual dysfunction, and seborrheic dermatitis
• A general feeling of weakness, malaise, or lassitude
• Depression or anhedonia
• Slowness in thinking

Plantar Heel Pain

Plantar heel pain is a commonly encountered orthopedic problem that can cause significant discomfort and a limp because of the difficulty in bearing weight. The etiologies of this condition are multiple; therefore, a careful clinical evaluation is necessary for its appropriate management. Nonsurgical or conservative care is successful in most cases.

Pathology
The specialized soft tissue at the heel functions as a shock absorber. The subcutaneous structure consists of fibrous lamellae arranged in a complex whorl containing adipose tissues that attach with vertical fibers to the dermis and the plantar aponeurosis.

An inflammatory response and reparative process can double the thickness of the plantar fascia, which is normally approximately 3 mm. Biopsy specimens reveal collagen necrosis, angiofibroblastic hyperplasia, chondroid metaplasia, and calcification.

The heel pain can also have a neurologic basis. The tibial nerve, with nerve roots from L4-5 and S2-4, courses in the medial aspect of the hindfoot, through the tarsal tunnel, under the flexor retinaculum, and over the medial surface of the calcaneus. The calcaneal branch, arising directly from the tibial nerve, carries sensation from the medial and plantar heel dermis. The tibial nerve and its branches in the hindfoot can be involved with compressive neuropathies. A valgus heel can stretch in the tibial nerve.

Clinical Presentation
A careful history and physical examination is valuable in identifying the etiology of heel pain. Taking a comprehensive medical and general history is important in order to distinguish between various causes.
The most common cause of plantar heel pain in both athletic and nonathletic populations is proximal plantar fasciitis.

• The discomfort commonly manifests spontaneously and insidiously without an antecedent trauma or fever. Occasionally, some patients state they might have stepped on a small object such as a pebble or they may have recently started an exercise regimen involving walking or running.
• The pain is localized to the plantar and medial aspects of the heel. It is worse typically with the first few steps in the morning. The pain causes patients to limp for approximately half an hour. It is also worse after a period of rest, such as after standing up from a chair or getting out of a car.
• An acute onset of pain, especially after a vigorous or sudden athletic activity, can be indicative of traumatic rupture of the plantar fascia.
• Fat pad atrophy in elderly patients and in persons who have received multiple steroid injections manifests with pain under the heel that is more diffuse, involving most of the weight-bearing surface.
• Pain radiating from the heel distally or proximally and associated with numbness, paresthesia, or a burning sensation after activity and continuing even after rest is likely to be neurologic in origin.
• Significant loss of appetite and weight or pain at night can be indicative of a neoplasm.

Managing Head Injuries

Head injury can be defined as any alteration in mental or physical functioning related to a blow to the head. Loss of consciousness does not need to occur.

Head injury refers to trauma of the head. This may or may not include injury to the brain.

Acute Management
In the setting of acute head injury, give priority to the immediate assessment and stabilization of the airway and circulation.

Following stabilization, direct attention to prevention of secondary injury. Keep mean arterial pressures above 90 mm Hg; arterial saturations should be greater than 90%. Urgent CT scanning is a priority.

Most head injuries are of a benign nature and require no treatment beyond analgesics and close monitoring for potential complications such as intracranial bleeding. If the brain has been severely damaged by trauma, neurosurgical evaluation may be useful.

Monitoring Intracranial Pressure
Since elevated intracranial pressure is an independent predictor of poor outcome. If the intracranial pressure rises above 20-25 mm Hg, intravenous mannitol, CSF drainage, and hyperventilation can be used. Hypertonic saline has also been used in lieu of mannitol to lower intracranial pressure.

Introduction to Pernicious Anemia

Pernicious anemia is a decrease in red blood cells that occurs due to impaired absorption of vitamin B-12 because of a lack of intrinsic factor (IF) in gastric secretions.

It occurs as a relatively common adult form of anemia that is associated with gastric atrophy and a loss of IF production and as a rare congenital autosomal recessive form in which IF production is lacking without gastric atrophy.

By definition, pernicious anemia refers specifically to vitamin B-12 deficiency resulting from a lack of production of IF in the stomach.

Causes: Common causes of pernicious anemia include:

• Weakened stomach lining (atrophic gastritis)
• An autoimmune condition in which the body’s immune system attacks intrinsic factor protein or the cells that make it.

Very rarely, pernicious anemia is passed down through families. This is called congenital pernicious anemia. Babies with this type of anemia do not make enough intrinsic factor or cannot properly absorb vitamin 12 in the small intestine.

Pathology
Vitamin B12 cannot be produced by the human body, and must be obtained from the diet. Normally, dietary B12 is absorbed by the body in the small bowel only when it is bound by the intrinsic factor (IF) produced by parietal cells of the gastric mucosa. Pernicious anemia is thought to occur when the body’s immune system mistakenly targets the IF, with a loss of parietal cells. Insufficient IF results in insufficient absorption of the vitamin. Although the normal body stores three to five years’ worth of B12 in the liver, the usually undetected autoimmune activity in one’s gut over a prolonged period of time leads to B12 depletion and the resulting anemia. Inhibition of DNA synthesis in red blood cells results in the formation of large, fragile megaloblastic erythrocytes.