Number 1 post: PG
Parkinson’s disease (PD), an advancing neurodegenerative disorder. Is the second (leading) neurodegenerative disorder behind Alzheimer’s disease (Vice, 2020). Genetics and environmental influences increase the risk of the illness (Vice, 2020). A deficiency in dopamine, a neurotransmitter, is the cause of the deterioration (Emamzadeh & Surguchov, 2018). Moreover, MacMahon Copas et al. (2021) described this disease as neuroinflammation, degeneration of dopaminergic neurons in the substantia nigra pars compacta. And the accumulation of misfolded synuclein proteins in Lewy bodies and neurites.
Moreover, microglia and astrocytes play a vital role in maintaining homeostasis within the central nervous system (CNS). Including protecting the gliosis (MacMahon Copas et al., 2021). In this discussion, how does bradykinesia manifest? What causes postural instability in this patient? Compare and contrast pyramidal versus extrapyramidal. And compare and contrast myelinated and unmyelinated fibers.
How does bradykinesia manifest?
One of the clinical findings in Parkinson’s disease is bradykinesia. Bradykinesia is the motor decline one sees in the Parkinson’s disease patient. According to Dlugasch and Story (2021), the manifestation of the disorder varies depending on the dopamine decline. Dlugasch and Story (2021 informed that the disorder’s generalized sluggish movement is known as bradykinesia. Also, bradykinesia in Parkinson’s disease may show in individuals as difficulty with gait, loss of dexterity, for instance, typing or buttoning clothes, and tying shoelaces (Dlugasch & Story, 2021).
Bologna et al. (2020) informed that bradykinesia clinical assessment is presently based on the MDS Unified Parkinson’s Disease Rating Scale, part III (Bologna et al., 2021: Goetz et al., 2008). Additionally, Dlugasch and Story (2021) discussed that with this disease, approximately 80% of patients with Parkinson’s typically occurs in the limbs at rest (resting tremors). However, finger-thumb rubbing (pill-rolling) could also be present (Dlugasch & Story, 2021).
What causes postural instability in this patient?
Postural instability appears later in the disease, and postural instability means not maintaining balance or homeostasis in one’s movement. Appeadu & Gupta (2021) state that “postural instability is the inability to maintain equilibrium under dynamic and static conditions such as preparation movements, perturbations, and quiet stance.” (Para 2). The condition
occurs due to hypo-dopamine in the brain. Moreover, the basal ganglia are involved (which plays a role in maintaining balance), and there are hypo-dopaminergic conditions with Parkinson’s disorder (Appeadu & Gupta, 2021). In essence, the patient could result in falls due to the motor impairment caused by the disease. Dlugasch and Story (2021) indicated that normal postural reflexes maintain balance; however, in Parkinson’s, the reflexes are eventually lost, and the patient could have falls that result in disability.
Compare and contrast pyramidal versus extrapyramidal.
According to de Oliveira-Souza (2017), pyramidal refers to motor neurons originating in the cerebral cortex. The neurons (pyramidal track) pass thru the medulla, and they function as voluntary (only) control of muscles in the body (de Oliveira-Souza 2017). In contrast, the extrapyramidal focus is on the involuntary and automatic controls in muscles such as tone, posture, balance, and locomotive (de Oliveira-Souza, 2017). The difference is pyramidal controls voluntary, and extrapyramidal can do more functions. Other extrapyramidal functions include inhibiting involuntary movements such as hyperkinesias and assisting in making voluntary movements more natural (Lee & Muzia, 2021). Both are involved as motor neurons that are pathways to send signals to lower neurons (de Oliveira-Souza, 2017).
Myelinated and unmyelinated fibers
Myelination is vital in determining the repair and regeneration of nerve cell fibers
due to injury (Arcilla & Tadi, 2017). Schwann cells that produce myelin (in the brain’s white matter) allow faster conduction of impulses versus unmyelinated cells (Arcilla & Tadi, 2017). Unmyelinated cells, there is no insulation of myelin; however, due to the unmyelinated cells, they are more excitable, thermosensitivity, and mechanosensitivity (Arcilla & Tedi, 2017).
In closing, Parkinson’s disease (a slow movement disorder) is the second leading cause of the neurodegenerative disorder behind Alzheimer’s disease. The condition is caused by the loss of cells in the brain that produce dopamine (cells in the substantia nigra of the brain). The disease will manifest bradykinesia, postural instability, and deficient myelinated cells. The disorder affects the muscular system and brain pathways to conduct impulses to muscle cells in the body.
Number 2 post: RB
Case Study: A 20-year-old female presents with severe migraines. She has been treated for the last two years.
In this case study, major problem of 20-year-old female is Migraine, which is an episodic primary headache disorder that can cause severe throbbing pain or a pulsing sensation, usually on one side of the head (unilateral). It’s often accompanied by nausea, vomiting, and extreme sensitivity to light and sound (Stephen, 2021). Migraine attacks can last for hours to days, and the pain can be so severe that it interferes with your daily activities.
What is the pathophysiology involved with the prodrome associated with migraines?
Migraine is thought to be a neurovascular pain syndrome with altered central neuronal processing (activation of brain stem nuclei, cortical hyperexcitability, and spreading cortical depression) and involvement of the trigeminovascular system (triggering neuropeptide release, which causes painful inflammation in cranial vessels and the dura mater). A prodrome (a sensation that a migraine is beginning) heralds attacks (Stephen, 2021).
The prodrome manifestations are often related to affective changes and can include mood changes, euphoria, yawning, neck pain, constipation, food cravings, loss of appetite, nausea, or a combination. The prodrome can occur 1-2 days prior to the onset of the headache (Dlugasch & Story, 2021). Many potential migraine triggers have been identified as: Drinking red wine, skipping meals, Excessive afferent stimuli (e.g., flashing lights, strong odors), Weather changes, Sleep deprivation, Stress, Hormonal factors, particularly menstruation and Certain foods (Stephen, 2021).
Compare and contrast tension headache and cluster headache. Use patho principles.
Tension-type headaches are a common headache often causing mild-to-moderate pain, which some describe as feeling like a tight band around their head. Tension headaches are frequently associated with fatigue, stress or hangovers. They generally respond to simple measures such as rest or over-the-counter pain medicine.
A characteristic of tension headaches is that pain usually occurs on both sides of head and is in the form of a dull, steady ache. Tension-type headache are more common in females. Tension-type headaches occur as a result of hypersensitivity of nerve fibers (Dlugasch & Story, 2021). Potential triggers for Tension-type headache includes: Sleep disturbances, Stress, Temporomandibular joint dysfunction, Neck pain and Eye strain.
Cluster headaches cause excruciating, unilateral periorbital or temporal pain, with ipsilateral autonomic symptoms (ptosis, lacrimation, rhinorrhea, nasal congestion). In other words, cluster headaches are rare, extremely painful and debilitating headaches that occur in groups or clusters. They often appear during seasonal changes.
They are also described as suicide headaches. A reference to the excruciating pain and resulting desperation that has sometimes culminated in actual suicide. Cluster headaches are more common in men. Pathophysiology of cluster headaches is unknown, but the periodicity suggests hypothalamic dysfunction and inflammation of the walls of the cavernous sinus, which injures sympathetic fibers that traverse in the sinus (Dlugasch & Story, 2021). Alcohol intake triggers cluster headache during the attack period but not during remission.
What is the pathophysiologic difference between migraine headache and tension headache?
A migraine is more likely to cause more severe pain/ throbbing. Or pounding pain, unilateral, gets worse when near bright lights. Or loud sounds and accompanied with nausea or vomiting. Migraine occurs as a result of vascular changes due to inflammation around the meninges (Dlugasch & Story, 2021). The migraine headache most likely originates in the sensory fibers innervating intracranial and extracranial blood vessels. Peripheral and central sensitization of trigeminovascular nociceptive pathways may develop during migraine attacks. Central sensitization of second- and third-order trigeminovascular nociceptive neurons may lead to transformation of episodic migraine to chronic migraine (Sait, Lars & Messoud, 2012). Whereas, Tension-type headache causes mild-to-moderate generalized pain (usually viselike) without the incapacity, nausea, or photophobia associated with migraine.
Tension-type headaches occur as a result of hypersensitivity of nerve fibers (Dlugasch & Story, 2021). Pericranial myofascial pain sensitivity is increased in patients with tension-type headache. And may be of importance in the pathophysiology of this headache. Sensitization of second-order neurons at the level of the spinal dorsal horn or trigeminal nucleus, sensitization of supraspinal neurons, and decreased descending inhibition from supraspinal structures play a major role in the pathophysiology of chronic tension-type headache (Sait, Lars & Messoud, 2012).