Gestalt Psychology and the Laws of Perceptual Organization

Gestalt psychology emerged as a response to structuralism, which aimed to break down thoughts into their basic components. Instead, Gestalt psychologists recognized that individual items must be examined together, as they interact and add complexity to the overall picture. Max Wertheimer, Kurt Koffka, and Wolfgang Köhler are important names associated with Gestalt psychology. Wertheimer discovered the phi phenomenon, which explains how rapid sequences of perceptual events create the illusion of motion. The Gestalt laws of perceptual organization explain how we tend to organize parts into wholes. These laws include symmetry and order, similarity, proximity, continuity, closure, and common fate. These laws help us understand how the mind groups similar elements into collective entities of totalities, and how spatial or temporal grouping of elements may induce the mind to perceive a collective of totality. Additionally, the laws explain how points that are connected by straight of curving lines are seen in a way that follows the smoothest path, and how things are grouped together if they seem to complete a picture. Finally, elements with the same moving direction are perceived as a collective of unit.

Research has shown that there is a connection between idiopathic rapid eye movement (REM) sleep behavior disorder (IRBD) and the onset of neurodegenerative diseases that involve alpha synucleinopathy, such as Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple systems atrophy (MSA).

Lesch-Nyhan Syndrome: A Rare Genetic Disorder

Lesch-Nyhan syndrome is a rare genetic disorder that causes the overproduction and accumulation of uric acid in the body, leading to various health problems such as gouty arthritis, kidney stones, and subcutaneous tophi. The condition primarily affects males and is caused by mutations in the HPRT gene located on the X-chromosome.

People with Lesch-Nyhan syndrome typically experience motor disability, including severe dystonia, hypotonia, and choreoathetosis, which can make it difficult of impossible for them to walk of sit without assistance. They may also exhibit self-injurious behavior, such as biting and head-banging, which is the most common and distinctive behavioral problem associated with the condition. Intellectual disability is common, but severe cognitive impairment is rare.

The absence of the HPRT enzyme, which is responsible for recycling purine bases, leads to the accumulation of uric acid and affects the development of specific neural pathways in the brain, particularly the mesotelencephalic dopamine pathways. This disruption is likely responsible for the motor disability and behavioral peculiarities associated with the condition.

Treatment for self-injurious behavior typically involves the use of protective restraints applied to the limbs, trunk, of head to prevent self-hitting of self-biting. Dental extraction may be necessary in cases of lip of tongue biting. Behavior modification methods that involve extinction may also be used, but neuroleptics may be required during particularly stressful of difficult behavior periods. However, these medications should only be used transiently due to their sedative effects and potential side-effects.

If mild cognitive impairment (MCI) does not affect driving, there is no need to inform DVLA. However, if there are concerns about the impact of MCI on driving, DVLA should be notified to conduct an investigation.

DVLA guidelines state that assessing driving ability in individuals with dementia is challenging. Those with poor short-term memory, disorientation, lack of insight, and judgment are likely to be unfit to drive. The varying presentations and progression rates of dementia are recognized, and attention disorders can also impair driving ability. Medical reports are typically used to determine fitness to drive. In cases of early dementia where sufficient skills are retained and progression is slow, a license may be granted, subject to annual review. A formal driving assessment may be necessary.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

It is probable that this individual has experienced a traumatic injury affecting the accessory nerve.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

QTc Prolongation: Risks and Identification

The QT interval is a measure of the time it takes for the ventricles to repolarize and is calculated from the beginning of the QRS complex to the end of the T wave. However, the QT interval varies with the heart rate, making it difficult to use a single number as a cut-off for a prolonged QT. Instead, a corrected QT interval (QTc) is calculated for each heart rate using various formulas. A QTc over the 99th percentile is considered abnormally prolonged, with approximate values of 470 ms for males and 480 ms for females.

Prolonged QT intervals can lead to torsade de pointes (TdP), a polymorphic ventricular tachycardia that can be fatal if it degenerates into ventricular fibrillation. TdP is characterized by a twisting of the QRS complexes around an isoelectric line and is often asymptomatic but can also be associated with syncope and death. An accurate diagnosis requires an ECG to be recorded during the event. It is important to note that an increase in the QT interval due to a new conduction block should not be considered indicative of acquired LQTS and risk for TdP.

Studies have demonstrated that memantine possesses neuroprotective properties for individuals with Alzheimer’s disease and those who have suffered from traumatic brain injury.

Pharmacological management of dementia involves the use of acetylcholinesterase inhibitors (AChE inhibitors) and memantine. AChE inhibitors prevent the breakdown of acetylcholine, which is deficient in Alzheimer’s due to the loss of cholinergic neurons. Donepezil, galantamine, and rivastigmine are commonly used AChE inhibitors in the management of Alzheimer’s. However, gastrointestinal side effects such as nausea and vomiting are common with these drugs.

Memantine, on the other hand, is an NMDA receptor antagonist that blocks the effects of pathologically elevated levels of glutamate that may lead to neuronal dysfunction. It has a half-life of 60-100 hours and is primarily renally eliminated. Common adverse effects of memantine include somnolence, dizziness, hypertension, dyspnea, constipation, headache, and elevated liver function tests.

Overall, pharmacological management of dementia aims to improve cognitive function and slow down the progression of the disease. However, it is important to note that these drugs do not cure dementia and may only provide temporary relief of symptoms.

The gamma secretase complex, consisting of four key proteins including presenilin, plays a crucial role in converting Amyloid Precursor Protein to Amyloid β-protein. Amyloid β-peptides are the primary components of the amyloid plaques found in the brains of individuals with Alzheimer’s disease. In the brain, APP is primarily cleaved by β-secretase, while in other tissues it is cleaved by α-secretase, followed by γ-secretase. The presence of the APOE4 allele is associated with a higher likelihood of developing Alzheimer’s dementia later in life.