Sandbox:nou

Dr Norina Usma

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Overview

Orthostatic hypotension is a physical finding demarcated by the American Academy of Neurology and the American Autonomic Society as a reduction in systolic blood pressure of 20 mm Hg or a drop of 10 mm Hg in diastolic blood pressure within three minutes of standing compared with blood pressure from the sitting or supine position. Orthostatic hypotension is frequently found in frail patients and those who are older.2 It is noticed in up to 20 percent of patients older than 65 years .

Classification

Initial orthostatic hypotension (iOH)

It is most common in healthy adolescents and is demarcated as a brief BP decrease of >40 mmHg systolic or >20 mmHg diastolic with symptomatic cerebral hypoperfusion within five to fifteen seconds after standing, typically resolves by twenty seconds.

Neurogenic orthostatic hypotension (nOH)

In Neurogenic orthostatic hypotension, the sympathetic noradrenergic nerves continually fail to facilitate the reflexive cardiovascular responses essential to sustain blood pressure in response to orthostatic stress. It is described as a constant BP decrease of >20 mmHg systolic or >10 mmHg diastolic, without or with symptoms, within three minutes of head-up tilt or standing.

Delayed orthostatic hypotension (dOH)

Delayed orthostatic hypotension (dOH) is demarcated as a fall in blood pressure that accomplishes neurogenic orthostatic hypotension criteria but ensues after three minutes.

Neurally mediated syncope (vOH)

It is also recognized as vasodepressor or vasovagal syncope, It involves a paroxysmal extraction of sympathetic vasopressor tone, frequently during prolonged standing, in patients with an effective autonomic nervous system.

Cardiovascular orthostatic hypotension (cOH)

Cardiovascular orthostatic hypotension occurs from intravascular hypovolemia or reduced cardiac output along with compensatory tachycardia.

Orthostatic pseudohypotension (pOH)

It is stated as apparent orthostatic hypotension when baseline supine blood pressure is raised, which may be due to a short time at rest to create a valid baseline, related recumbent hypertension, or fluctuation of baseline blood pressure with labile hypertension.

Pathophysiology

• In standing position, 300 to 800 mL of blood pools in the lower extremities. Preservation of blood pressure while changing the position requires many organs like cardiac, neurologic, vascular, muscular, and neurohumoral to respond rapidly.9 If any of these responses are irregular, organ perfusion and blood pressure can be reduced. Therefore, symptoms of central nervous system hypoperfusion may arise, including nausea, weakness, dizziness, headache, lightheadedness, fatigue, blurred vision, palpitations, tremulousness, vertigo, and impaired cognition.
• The autonomic nervous system plays a significant role in sustaining blood pressure when a person changes position. The sympathetic nervous system regulates the tone in the heart, arteries, and veins.
• Baroreceptors located mainly in the aorta and carotid arteries are very sensitive to fluctuations in blood pressure. As soon as the baroreceptors sense the minor decrease in blood pressure, a synchronized increase in sympathetic stimulation occurs. Arteries contract to increase blood pressure and peripheral resistance, and subsequently increases heart rate and contractility.
• All of these responses are designed to sustain perfusion and blood pressure. Additional physiologic mechanisms can also be involved including the renin-angiotensin-aldosterone system, low-pressure receptors in the heart and lungs, the systemic release of norepinephrine, and vasopressin.
• Over-all, all parts of the nervous systems and cardiovascular must work together. If there is insufficient intravascular volume, a decrease of venous return, impairment of the autonomic nervous system, or the heart's incapability to pump with the higher power, orthostatic hypotension may result.

Causes

Common causes of Apraxia may include:

• It could be due to a defect in the brain pathways that comprise memory of learned forms of movement.
• Any disease that is related to these areas can lead to apraxia, stroke, dementia are the leading causes, but there are many other causes as well.
• The lesion cause could be because of certain metabolic, neurological, or other disorders that influence the brain, predominantly the frontal lobe, inferior parietal lobule of the left hemisphere of the brain. In this area, complex, 3-dimensional depictions of formerly learned patterns and movements are stored</ref>.
• Patients with apraxia cannot regain these representations of stored, skilled actions.Therefore, patients with apraxia are unable to perform daily living activities well.

Differentiating Xyz from Other Diseases

Childhood apraxia of speech (CAS)	Neuropraxia	Dyspraxia	Dysarthria	Aphasia
CAS is a neurological childhood speech disease in which the consistency and precision of speech movements are weakened without neuromuscular deficits. CAS is also known as verbal dyspraxia or developmental apraxia.	Neuropraxia is the disease of traumatic peripheral nerve injury. It is categorized by focal segmental demyelination at the injury site, which results in obstruction of nerve conduction and transient paresthesia or weakness	Dyspraxia is defined as the breakdown of actions and the inability to apply voluntary motor activities effectively in all parts of life from play to organized, skilled responsibilities	Dysarthria is a motor speech illness and is associated with troubles of laryngeal function, respiration, articulation, and airflow direction leading to difficulties of speech intelligibility and quality.	Aphasia is a condition having trouble with the formulation and comprehension of language triggered by dysfunction in the precise brain region.

Epidemiology and Demographics

Incidence

Apraxia is the common complication of left-brain damage that leads to a deficiency in performing motions to verbal imitation or command. Patients suffering from Limb apraxia are mainly impaired when asked to validate how to use an object or perform actions involving. Epidemiology studies account that Ideomotor Apraxia is present 13% of right-brain–and in 28% of left-brain damaged patients, during the acute stage of stroke.Ideomotor apraxia incidence is 34% of right-brain and 57% of left- brain-damaged patients. Ideomotor apraxia persisted to some degree in 45% of patients one year after stroke onset.

Prevalence

Prevalence rates of  apraxia range among 0 and 34% for patients with Right hemisphere stroke and 28–57% for patients with Left hemisphere stroke.Real tool-use loss prevalence rates were stated with 25–54% impaired level of patients

Age

Apraxia commonly affects individuals older than 50 years of age.

Gender

Apraxia affects men and women equally.

Risk Factors

Apraxia is a rare disease that tends to affect patient population at high risk of having stroke and Alzheimer disease. Stroke is the major cause of stroke and it is more common in older people. Risk factors for apraxia are similar as risk factors of stroke which include

• High blood pressure
• High cholesterol
• Diabetes
• Smoking
• Prior stroke or cardiovascular disease
• Prior transient ischemic attack (TIA)
• Dialysis treatment

Screening

There is insufficient evidence to recommend routine screening for apraxia.

Natural History, Complications, and Prognosis

• The symptoms of apraxia typically develop during early or later years depending on the cause and the location affected.
• Often, patients with apraxia are not aware of their shortfalls. Therefore, the history of a patient's capability to accomplish skilled movements should be obtained from the patient's caregiver or the patient himself.
• Caregivers should be asked about the capability of patients to perform activities of daily living and perform tasks involving household tools such as using a toothbrush, knife, and fork appropriately, using kitchen utensils correctly and safely to prepare a meal; using tools such as scissors or hammer correctly.
• Caregivers should also be asked about the whole activity level of the patient and whether decreases in his or her total actions have happened.
• The patient may sit on the couch and watch television without showing interest in essential activities he or she use to do in the past.
• This indifference can be related to many kinds of brain dysfunction, but it sporadically occurs because the patient is incapable of performing his or her usual activities.

Complications

Common complications of apraxia include:

• Broca's Aphasia
• Acalculi
• Right-left Confusion
• Alexia with agraphia
• Wernicke's Aphasia.

Prognosis

• Depending on the extent of the Apraxia progression at the time of diagnosis, the prognosis may vary.
• Prognosis of apraxia differs and depends partially on the original cause.
• Some people improve while others may display minimal improvement.
• Over-all, patients with apraxia rely on others for their daily activities and need at least some notch of command; skilled nursing care may be obligatory.
• Patients with the tumor or degenerative diseases usually develop into amplified levels of dependence.
• Patients with stroke may have a steady progression and may even recover somewhat.
• Persistence of apraxia of speech after 12 months is related to a larger volume of the left hemispheric stroke connecting Broca's area.
  

Diagnostic Study of Choice

• There is no single diagnostic study of choice for Apraxia's diagnosis, but Apraxia can be diagnosed based on neuroimaging and activity of daily living.
• When diagnosing Apraxia, specialists may look for the manifestation of other symptoms. For example, they may look for difficulties or weaknesses with verbal comprehension. Both of these are suggestive of other conditions, and their occurrence would support rule out Apraxia.
• For people with potential acquired Apraxia, they should go through neuroimaging—magnetic resonance imaging (MRI) or computed tomography (CT) scanning MRI which may be beneficial to determine the location and extent of any brain damage. It will also help evaluate possible atrophy expressive of a degenerative condition and exclude a mass lesion.
• Whitwell et al. in a study to determine the metabolic and neuroanatomical relate to aphasia and progressive Apraxia of speech (AOS), associations between the Token Test to assess Aphasia, Western Aphasia Battery and AOS rating scale (ASRS), 18-F fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging and 3-Tesla MRI, were assessed. The only region that interconnected to ASRS was left-superior promotor volume.
• A broad assessment of Apraxia should consist of observation of daily routines, formal testing, self-report questionnaires, standardized measurements of ADLs, and targeted interviews with the patients and their relatives . Apraxia should not be mixed up with aphasia (the inability to understand language); though, they often occur together.

Physical Examination

Physical examination of patients with Apraxia is usually dependent on what type of Apraxia they have for example Ideomotor apraxia, Buccofacial apraxia, and Constructional apraxia.

Ideomotor apraxia:

• Patients with ideomotor apraxia are tested based on the physical examination performed at the bedside with simple tests for the capability to use tools.
• The examiner requests patients to achieve three types of activities.
• For example, the patient is asked to hammer a nail into the (unreal) wall in front of them; patients are given a pair of scissors to cut a piece of paper.
• However, different pantomimes could be made, including cutting with a saw, brushing teeth, peeling a potato or whipping eggs with an eggbeater.
• Any error in carrying out the above activities indicates a loss of familiarity about the movement to be completed.
• The response is recorded as an error.

Buccofacial apraxia:

• Patients cannot do skilled actions.

Constructional apraxia:

• Failure to copy or draw quality images.
• Localizes lesions involving frontal or parietal area.

Electrocardiogram

There are no ECG findings associated with Apraxia.

X-ray

There are no x-ray findings associated with Apraxia.

Echocardiography and Ultrasound

There are no echocardiography/ultrasound findings associated with Apraxia.

CT scan

Brain CT scan may be helpful in the diagnosis of Apraxia. Findings on CT scan suggestive of/diagnostic of Apraxia include

• To look for a mass lesion and
• To evaluate for possible atrophy expressive of a degenerative condition.

MRI

Brain MRI may be helpful in the diagnosis of Apraxia. Findings on MRI suggestive of/diagnostic of Apraxia include atrophy, ischemic changes, and mass lesion.

Other Imaging Findings

There are no other imaging findings associated with Apraxia.

Other Diagnostic Studies

Diagnostic study PET may be helpful in the diagnosis of Apraxia. Findings suggestive of/diagnostic of Apraxia include Relative cerebral glucose metabolism.

Treatment

Medical Therapy

The mainstay of treatment for Apraxia is various therapy.

Interventions

There are no specific recommended therapeutic interventions for the management of Apraxia.

Apraxia is believed to have an adverse impact on the Activity of Daily Living independence. There are limited information and research available regarding various treatments</ref>. Various interventions include:

• Daily living doings training: this method explains internal and external compensatory approaches that permit a functional mission to be accomplished.
• Sensory Stimulation: Including deep pressure stimulation, soft and sharp touch are useful to the patients' limbs.
• Chaining (forward or backward): This method is fragmented down into its sections. The task is done with assistance from the therapist separately from the final element through backward chaining, which the patient performs out unassisted. If positive next time, additional steps are presented. Forward chaining is the opposite of backward chaining;
• Proprioceptive stimulation: The patient props on and puts his weight through their upper and lower extremities;
• Cueing, physical or verbal stimuli: This technique enables each phase of the task to be completed;

Surgery

Surgical intervention is not recommended for the management of Apraxia.

Primary Prevention

There are no established measures for the primary prevention of Apraxia. It is difficult to prevent this acquired condition which is mostly linked to stroke. Following measures to prevent a stroke may help. Some steps include:

• Exercise regularly.
• Eat a healthy diet.
• Limit how much alcohol you drink.
• Quit smoking
• Check your blood pressure often.

Secondary Prevention

Secondary prevention of stroke is the mainstay of preventing Apraxia as it is the leading cause of the various type of Apraxia. Effective measures for the secondary prevention of Apraxia include:

• Aspirin, clopidogrel, extended-release dipyridamole, ticlopidine
• Anticoagulants (apixaban, dabigatran, edoxaban, rivaroxaban, warfarin)
• Blood pressure-lowering medications.
• Diabetes Control
• Low-fat diet
• Cholesterol-lowering medications, Cessation of cigarette smoking, carotid revascularization

• Weight loss and Exercise