Figure 1.indicates the level of ‘brain activity’ in both the ‘depressed’ & ‘non-depressed’ brain. It is fairly clear that there is a significant loss of neurotransmitter activity in the depressed individual’s brain functioning. The primary areas affected are those relating to ‘mood’, ‘emotions’, ‘motor activity’, ‘cognitive functioning’, ‘sex drive’, ‘appetite’ & ‘sleep’. In depression, two (2) main neurotransmitters are involved; Serotonin, & Norepinephrine. Most medication interventions (anti-depressants) ‘target’ these neurotransmitters with the aim of increasing neuronal, synaptic activity or ‘normalizing’ functioning within the synapses. There may be situations where ‘hormonal imbalances’ and other physiological anomalies have resulted in depression or depressive symptoms. In these cases, the appropriate interventions are undertaken with the same intention; that of restoring the functioning within the brain; to ‘normality’. Depression is generally ‘treatable’ and many of the observable ‘reduced activities’ can be reversed. Problems arise when the physical changes in biochemistry &/or structure of the brain is such that ‘standard’ methodology is ineffective. This may apply to many ‘organic’, ‘congenital’,’ heredity-based’ or ‘non-reversible’ causes, such as trauma or drug/alcohol abuse. Some of these conditions are noted further in this section.

Figure 1

Despite low levels of the neurotransmitter ‘GABA’  having been identified as providing a neurological/chemical basis for epilepsy, about 75% of cases cannot be attributed to any specific cause. GABA is a primary ‘inhibitory neurotransmitter’ in the synapses and low levels can result in a greater susceptibility to seizures when there is insufficient to slow down or control electrical activity within the neuronal pathways, allowing the ‘excitatory’ neurotransmitters to perpetuate the signal. There are many possible reasons for the development of epilepsy. These may be hereditary or genetic factors, illness, injury or trauma. In the case of the latter, head injuries can be a precursor to epilepsy & this particularly applies to those who participate in sports where there is high level body contact or a greater likelihood of head injury or concussion. 

Memory loss (particularly short term), behavioural changes, cognitive difficulties, loss of inhibition or initiative, are but some of the initial signs of Alzheimer’s Disease. Whilst it is a ‘dementia’ it is not part of the ‘normal’ aging process, despite the incidence being greater as one ages. There are many theories as to the origins of the disease, though certain neurological facts have been noted as being common among all sufferers. The most significant is the irreversible, degenerative changes in neurons. Nerve-cell loss, abnormal ‘tangles’ within the cells and chemical and neurotransmitter deficiencies are typical of the disease. As the disorder progresses, increased behavioural & personality changes are noted, along with significant memory problems, confusion & disorientation, gross & fine motor activity difficulties and sometimes ‘paranoia’. Eventually, physical deterioration leads to total dependence and immobility. There are five (5) general theories in relation to cause s&/or origins of the disease; Chemical, Genetic, Autoimmune, Slow Virus & Blood Vessel theory. Neurotransmitters implicated in Alzheimer’s disease are Acetylcholine, Somatostatin, monoamines & Glutamate; with marked reduction in each. There is currently no known cure for the disease, despite advances in identification, genetics & biochemistry. 

The picture on the right are 'actual brains' and indicate the comparison between the Alzheimers brain & the normal brain.

Tourette Syndrome (TS) is an inherited (genetic) neurological movement disorder that involves ‘involuntary’ behaviours & muscle activity known as ‘tics’. The average age for manifestation or onset of TS is around 7 years and generally before the age of 18. The incidence of TS is three (3) to four (4) times greater in males and is a lifelong illness, with no known cure as yet. The most commonly seen ‘tics’ are those relating to ‘rapid & repetitive’ blinking, constant muffled coughing or clearing of the throat, sudden, and sometimes extreme, movements such as ‘jumping’ and the incongruous, ‘out of context’ vocal utterances of words or phrases. Despite the profound and obvious behaviours, TS is of a neurological origin rather than psychological. It originates from a chemical imbalance between Serotonin, Dopamine & Norepinephrine. Abnormalities in Norepinephrine in particular give rise to an increase in Dopamine, which in turn results in the sudden, involuntary movements & behaviours. TS is associated with other disorders such as OCD, ADHD, Dyslexia & sleep disturbances; the latter being attributed to Serotonin imbalance.  

  Huntington’s (chorea) is included in this section because of its uniqueness in ‘heredity’. A severe degenerative neurological disorder with extreme and tragic symptoms, Huntington’s is clearly identified within ‘families’ generationally. Initially described in 1872, it is caused by a dominant gene; which means that anyone inheriting this gene from their parents will develop the disease. Symptoms are generally observed in the individual’s mid-thirties, meaning many have already produced off-spring without knowledge of what awaits them. The two (2) primary neurotransmitters involved initially are Acetylcholine & GABA. This ultimately leads to the increase in Dopamine. Symptoms usually begin mildly; a degree of clumsiness, dropping things, deteriorated co-ordination. As the disorder progresses, marked changes and abnormalities occur with movement – sudden, bizarre, spontaneous involuntary actions. Eventually the brain shrinks, through atrophy (Figure 8), the ventricles enlarge (Figure 9) & dementia results.  

                      Figure 8                                                               F igure 9

Symptoms such as weakness, paralysis, numbness of limbs, tingling sensations, loss of, or disturbances to, vision, exhaustion or chronic fatigue, slurred speech, constant pain, balance & co-ordination problems, dysfunctional bladder & bowel control are many of the serious results of Multiple Sclerosis (MS). In the early stages, it is difficult to accurately diagnose MS due to the varied, somewhat minor symptoms initially experienced and it is only when those of a major and destructive nature appear that MS can generally be established. It is particularly tragic in its onset as about 2/3 of sufferers are between 20 & 40, being very rarely diagnosed in the elderly or young. The eventual outcome of MS can vary, depending on the severity of symptoms; from mild impairment to a severe degree and associated inability to function in any manner, severe cognitive impairment & total incapacitation for those who survive long enough. Whilst MS is a ‘neurological illness’, it is not related directly to neurotransmitter imbalances or dysfunction; rather, an ‘auto-immune’ disease where the body’s own immune system attacks normal bodily tissues, treating them as ‘foreign’ & attempting to destroy them as if they were an infection, virus etc. The primary target for this auto-immune response is the ‘brain & spinal’ tissues; and more specifically the ‘Myelin’ sheath or covering of the axons of neurons. This tissue is similar to insulation of electrical wiring. The inflammation that results either disrupts or destroys the axon, thus affecting the transmission of electrical impulses. Damaged axons are scarred and these regions develop ‘plaques’ as a result (Figure 12). The incidence of MS is significantly greater in women than men; at a ratio of approximately 2 : 1. There is no known ‘cure’ for MS, though advancements in treatment and research are encouraging. At present, however, the MS sufferer’s best scenario is either mild symptoms or ‘reasonable’ periods of remission.

  Figure 12

As with ‘depression’, change in brain activity is visible by use of scans. Figure 2. shows a ‘normal’ brain at the top with the ‘hypomanic’ (bipolar disorder) in the middle and the ‘depressed’ brain at the bottom. During a depressive phase of the bipolar, an individual might well present with the reduced activity as shown. Problems may arise when they are misdiagnosed and treated with an antidepressant medication. It can, not only lift a person from depression, but actually induce a ‘manic’ episode. Researchers have found a hypersensitivity to the neurotransmitter ‘acetylcholine’ along with a greater number of ‘cholinergic’ receptors in the brains of those with bipolar disorder. ‘Lithium’, often used in the treatment of bipolar is known to block or interfere with acetylcholine.

Brain Tumours can be ‘malignant’ or ‘benign’ and can also be termed ‘secondary’ metastases if resulting from the spread from the original source (cancer) through the blood stream. Irrespective of the type, all tumours can cause serious physical damage to the brain’s structure. In the instance of ‘Gliomas’ (generally malignant), the massive & toxic release of Glutamate destroys neurons to allow for the tumour’s growth. Surgery, radiation & chemotherapy are the only methods of treating Brain Tumours. Symptoms such as headaches or migraines, visual disturbances, seizures, vomiting, disturbed senses (smell, taste, hearing etc..) and general impaired cognitive & behavioural functioning are common, though some are dependant on the region of the brain affected. 

Autism can best be identified by criteria such as communication difficulties, impaired social abilities & skills, obsessive &/or repetitive behaviours, limited and obsessive interests and language problems (from mild, delayed, absent or abnormal). Those suffering Autism might also exhibit significant developmental & cognitive impairment or retardation, epilepsy and aberrant behaviours. Medical imaging & investigations suggest malformation in nerve pathways, neurons and brain structure both before & after birth. Serotonin and more specifically, the increase in the neurotransmitter is evidenced in Autism, though not the cause. The malfunctioning, unusual ‘wiring’ of the nerve pathways in sections of the brain are the primary causes.

The logo above is the ‘international’ symbol for Autism. 

A deficit in Dopamine is one of the most significant aspects noted in the neurodegenerative disease; Parkinson’s Disease. A deterioration in that part deep within the brain stem responsible for motor (movement) functioning results in symptoms such as hand, arm, leg, jaw & face tremors, along with psychomotor retardation (slow movement or gait) and balance & co-ordination problems. As the disease progresses, there are pronounced difficulties encountered with walking & talking. An imbalance in neurotransmitters Dopamine & Acetylcholine  appear to be the primary reasons for the disorder. When Dopamine levels drop significantly, Acetylcholine is similarly affected; thus resulting in the disturbances in movement. Secondary progressive features and symptoms appear to be related to Norepinephrine, Serotonin & GABA. Many theories abound as to the causes of Parkinson’s Disease, though as yet none are definitive. Permanent physiological and neurological changes to the brain structure such as damaged neurons are primary features of the disease. Treatment via medication is partially successful in the amelioration of the symptoms, but generally only temporarily, and it must be weighed up against the side effects of the drugs and the likelihood of ultimate ‘worsening’ in severity of the symptoms. Surgical procedures have also been undertaken with mixed results. 

‘The Greatest’– Muhammad Ali.  

The head injuries sustained during his career almost certainly resulted in the tragic development of Parkinson’s Disease.

A study in 1990, via means of ‘scans & imaging’, noted the lowered capacity to use ‘glucose’ in the ADHD brain. Glucose is the main source of energy for brain functioning & those areas particularly affected relate to ‘attention’, ‘motor control’, ‘handwriting’ & ‘inhibition’. ‘Birth trauma’, and ‘maternal drug &/or alcohol abuse’ may also contribute to the development of ADHD, though it is the brain’s chemical imbalances that are most significant. The two (2) primary neurotransmitters identified are ‘Dopamine’ & ‘Norepinephrine’. It is the ‘low’ levels of these neurotransmitters that appear to result in the behavioural and learning difficulties evident with the ADHD sufferer. The administration of ‘Ritalin’ or similar psycho-stimulants have been effective in raising the levels of Dopamine & reducing the manifested symptoms of the Disorder.

Causes of Schizophrenia are postulated to be many and varied. Developmental abnormalities through heredity or genetic predisposition; brain trauma; maternal infection and more recently the permanent effects of certain illicit substances that induce psychotic symptoms or that grossly affect the brain structure and/or neurotransmitters and synapses within the brain. Disordered thought, delusions, hallucinations, social withdrawal or socially inappropriate behaviours, incongruous emotional responses and reactions are some of the primary symptoms manifested in the disease. It is generally diagnosed between the ages of 15 & 25, with symptoms of social withdrawal & dysfunction, pre-occupation and noted deficits or decline in basic ADLs or hygiene. The early stages are often referred to as ‘Prodromal’. Neurotransmitters heavily associated with Schizophrenia are Dopamine, Glutamate & GABA. Approximately ¼ of all Schizophrenics do not recover to a point of relative social functionality; being considered ‘chronic’. The majority will experience life-long intermittent ‘episodic’ symptom manifestation, and the minority will be able to return to some degree of productivity. Symptoms are often described as ‘positive’ or ‘negative’. The psychotic features are generally ‘positive’ and the social withdrawal, apathy or emotional retardation/blunting are seen as ‘negative’ features. Medication, both ‘typical’ (Largactil, Serenace etc.) & ‘Atypical’ (Zyprexa, Seroquel, Risperidone etc.) are used in the treatment of the disease, though some ‘non-compliant’ Schizophrenics are treated with ‘Depot Medication’ (deep intramuscular slow release injections).