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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 [1][2][3].

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[4][5][6][7].

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[8][9][10][11][12].

Causes

Primary:

  • Parkinson disease
  • Pure autonomic failure
  • Multiple system atrophy
  • Autoimmune autonomic gangliopathy
  • Lewy body dementia
  • Rare Hereditary disorders (Familial dysautonomia, dopamine beta hydrolase deficiency)

Secondary:

  • Iatrogenic (drug-related,
  • Diabetes mellitus
  • Alcoholic polyneuropathy
  • Amyloidosis
  • Multiple myeloma
  • Endocrine Disease (adrenal insufficiency, thyroid disease, diabetes insipidus)
  • Cerebrovascular disease
  • Spinal cord disease
  • Paraneoplastic syndrome
  • Multiple sclerosis
  • Cardiovascular disease (sick-sinus syndrome, AV block, heart failure, aortic stenosis, pulmonary hypertension, essential hypertension)
  • Volume depletion, Venous pooling
  • Autoimmune disease

Differentiating Xyz from Other Diseases

Intravascular volume depletion: Blood loss Dehydration Pregnancy/postpartum Shock

Cardiovascular: Anemia Cardiac arrhythmia Congestive heart failure Myocardial infarction Myocarditis Pericarditis Valvular heart disease Venous insufficiency Postprandial hypotension

Neurologic Causes: Amyloidosis (hereditary and primary) Diabetic autonomic neuropathy Lewy body dementia Multisystem atrophy (Shy-Drager syndrome) Parkinson disease Pure autonomic failure

Drugs: Alcohol Antiadrenergics Antianginals Antiarrhythmics Anticholinergics Antidepressants Antihypertensives Antiparkinsonian agents Diuretics Narcotics Neuroleptics Sedatives

Endocrine Causes: Adrenal insufficiency Diabetes insipidus Hyperglycemia, acute Hypoaldosteronism Hypokalemia Hypothyroidism Pheochromocytoma

Miscellaneous: AIDS Anxiety or panic disorder Eating disorders Prolonged bed rest

Epidemiology and Demographics


For the WikiDoc page for this topic, click here Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2]

Differential diagnosis of headache includes: Migraine, tension-type headache, cluster headache, seizure, meningitis, encephalitis, neurosyphilis, SAH, subdural hematoma, brain tumor, hypertensive encephalopathy, brain abscess, multiple sclerosis, hemorrhagic stroke, Wernickes encephalopathy, and drug toxicity etc.[13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31]


Disease History and Physical Examination Diagnostic approach
Lightheadedness Fatigue Autonomic symptoms Fever Nausea/omiting Diminished Vision Dizziness Slurred Speech Tachycardia Altered mentation Loss of Consciousness Weakness Neurological Deficit Labs and CSF findings ECG CT/MRI Gold standard test
Multiple system atrophy with orthostatic hypotension + + + - - + + + - + - + + - - Atrophy of brain stem and cerebellum Clinical assesment
Neurally mediated hypotension + + + - + + + + - + - + - - - - Clinical assesment
Postural Orthostatic Tachycardia Syndrome (POTS) + + + - - - - - + - - - - - + - Clinical assesment
Neurologic syncope + - + - + +/- + - - - + +/- - - - - Clinical assessment
Cardiac syncope + + + _ + + + + + +/- + + - - + - ECG, Holter monitor, Echocardiography
Situational syncope + + + - + + + +/- +/- +/- + +/- - - - - Clinical assessment syncope occurs during defecation, micturition or coughing
Vasovagal syncope (also known as cardio-neurogenic syncope) + + + - + +/- + + - + + +/- - + + - ECG, Echo cardiogram, Exercise stress test.

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[32].
  • 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[33].
  • 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[34].
  • 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 [35]. 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[36].
Buccofacial apraxia:
  • Patients cannot do skilled actions.
Constructional apraxia:
  • Failure to copy or draw quality images.
  • Localizes lesions involving frontal or parietal area.

Laboratory Findings

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[37]. There are limited information and research available regarding various treatments[38]</ref>. Various interventions include:

  • Daily living doings training: this method explains internal and external compensatory approaches that permit a functional mission to be accomplished[39].
  • Sensory Stimulation: Including deep pressure stimulation, soft and sharp touch are useful to the patients' limbs[40].
  • 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[41]. 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[42]. 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

References

  1. ↑ Bradley JG, Davis KA (2003). "Orthostatic hypotension". Am Fam Physician. 68 (12): 2393–8. PMID 14705758.
  2. ↑ Rutan GH, Hermanson B, Bild DE, Kittner SJ, LaBaw F, Tell GS (1992). "Orthostatic hypotension in older adults. The Cardiovascular Health Study. CHS Collaborative Research Group". Hypertension. 19 (6 Pt 1): 508–19. doi:10.1161/01.hyp.19.6.508. PMID 1592445.
  3. ↑ Ooi WL, Barrett S, Hossain M, Kelley-Gagnon M, Lipsitz LA (1997). "Patterns of orthostatic blood pressure change and their clinical correlates in a frail, elderly population". JAMA. 277 (16): 1299–304. PMID 9109468.
  4. ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1007/s10286-016-0382-6 Check |pmid= value (help).
  5. ↑ Wieling W, Krediet CT, van Dijk N, Linzer M, Tschakovsky ME (2007). "Initial orthostatic hypotension: review of a forgotten condition". Clin Sci (Lond). 112 (3): 157–65. doi:10.1042/CS20060091. PMID 17199559.
  6. ↑ Freeman R, Wieling W, Axelrod FB, Benditt DG, Benarroch E, Biaggioni I; et al. (2011). "Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome". Clin Auton Res. 21 (2): 69–72. doi:10.1007/s10286-011-0119-5. PMID 21431947.
  7. ↑ Wieling W, Schatz IJ (2009). "The consensus statement on the definition of orthostatic hypotension: a revisit after 13 years". J Hypertens. 27 (5): 935–8. doi:10.1097/HJH.0b013e32832b1145. PMID 19390349.
  8. ↑ Lipsitz LA (1989). "Orthostatic hypotension in the elderly". N Engl J Med. 321 (14): 952–7. doi:10.1056/NEJM198910053211407. PMID 2674714.
  9. ↑ Low PA, Opfer-Gehrking TL, McPhee BR, Fealey RD, Benarroch EE, Willner CL; et al. (1995). "Prospective evaluation of clinical characteristics of orthostatic hypotension". Mayo Clin Proc. 70 (7): 617–22. doi:10.4065/70.7.617. PMID 7791382.
  10. ↑ Zaqqa M, Massumi A (2000). "Neurally mediated syncope". Tex Heart Inst J. 27 (3): 268–72. PMC 101078. PMID 11093411.
  11. ↑ Mathias CJ (1995). "Orthostatic hypotension: causes, mechanisms, and influencing factors". Neurology. 45 (4 Suppl 5): S6–11. PMID 7746371.
  12. ↑ Hollister AS (1992). "Orthostatic hypotension. Causes, evaluation, and management". West J Med. 157 (6): 652–7. PMC 1022100. PMID 1475949.
  13. ↑ "National guidelines for analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage". Ann. Clin. Biochem. 40 (Pt 5): 481–8. September 2003. doi:10.1258/000456303322326399. PMID 14503985.
  14. ↑ Le Rhun E, Taillibert S, Chamberlain MC (2013). "Carcinomatous meningitis: Leptomeningeal metastases in solid tumors". Surg Neurol Int. 4 (Suppl 4): S265–88. doi:10.4103/2152-7806.111304. PMC 3656567. PMID 23717798.
  15. ↑ Chow E, Troy SB (2014). "The differential diagnosis of hypoglycorrhachia in adult patients". Am J Med Sci. 348 (3): 186–90. doi:10.1097/MAJ.0000000000000217. PMC 4065645. PMID 24326618.
  16. ↑ Leen WG, Willemsen MA, Wevers RA, Verbeek MM (2012). "Cerebrospinal fluid glucose and lactate: age-specific reference values and implications for clinical practice". PLoS One. 7 (8): e42745. doi:10.1371/journal.pone.0042745. PMC 3412827. PMID 22880096.
  17. ↑ Negrini B, Kelleher KJ, Wald ER (2000). "Cerebrospinal fluid findings in aseptic versus bacterial meningitis". Pediatrics. 105 (2): 316–9. PMID 10654948.
  18. ↑ Brouwer MC, Tunkel AR, van de Beek D (2010). "Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis". Clin Microbiol Rev. 23 (3): 467–92. doi:10.1128/CMR.00070-09. PMC 2901656. PMID 20610819.
  19. ↑ Vermeulen M, Hasan D, Blijenberg BG, Hijdra A, van Gijn J (July 1989). "Xanthochromia after subarachnoid haemorrhage needs no revisitation". J. Neurol. Neurosurg. Psychiatry. 52 (7): 826–8. doi:10.1136/jnnp.52.7.826. PMC 1031927. PMID 2769274.
  20. ↑ Wasay M, Mekan SF, Khelaeni B, Saeed Z, Hassan A, Cheema Z, Bakshi R (June 2005). "Extra temporal involvement in herpes simplex encephalitis". Eur. J. Neurol. 12 (6): 475–9. doi:10.1111/j.1468-1331.2005.00999.x. PMID 15885053.
  21. ↑ Glaser CA, Honarmand S, Anderson LJ, Schnurr DP, Forghani B, Cossen CK, Schuster FL, Christie LJ, Tureen JH (December 2006). "Beyond viruses: clinical profiles and etiologies associated with encephalitis". Clin. Infect. Dis. 43 (12): 1565–77. doi:10.1086/509330. PMID 17109290.
  22. ↑ Meltzer EO, Hamilos DL (May 2011). "Rhinosinusitis diagnosis and management for the clinician: a synopsis of recent consensus guidelines". Mayo Clin. Proc. 86 (5): 427–43. doi:10.4065/mcp.2010.0392. PMC 3084646. PMID 21490181.
  23. ↑ Rasmussen BK, Jensen R, Schroll M, Olesen J (1991). "Epidemiology of headache in a general population--a prevalence study". J Clin Epidemiol. 44 (11): 1147–57. doi:10.1016/0895-4356(91)90147-2. PMID 1941010.
  24. ↑ Kelman L (October 2004). "The premonitory symptoms (prodrome): a tertiary care study of 893 migraineurs". Headache. 44 (9): 865–72. doi:10.1111/j.1526-4610.2004.04168.x. PMID 15447695.
  25. ↑ Laurell K, Artto V, Bendtsen L, Hagen K, Häggström J, Linde M, Söderström L, Tronvik E, Wessman M, Zwart JA, Kallela M (September 2016). "Premonitory symptoms in migraine: A cross-sectional study in 2714 persons". Cephalalgia. 36 (10): 951–9. doi:10.1177/0333102415620251. PMID 26643378.
  26. ↑ Charlotte E. Grayson and The Cleveland Clinic Neuroscience Center (October 2004). "Cluster Headaches". WebMD. Retrieved 2006-09-22.
  27. ↑ Drummond PD (October 1994). "Sweating and vascular responses in the face: normal regulation and dysfunction in migraine, cluster headache and harlequin syndrome". Clin. Auton. Res. 4 (5): 273–85. doi:10.1007/BF01827433. PMID 7888747.
  28. ↑ Drummond PD (June 2006). "Mechanisms of autonomic disturbance in the face during and between attacks of cluster headache". Cephalalgia. 26 (6): 633–41. doi:10.1111/j.1468-2982.2006.01106.x. PMID 16686902.
  29. ↑ Ekbom K (August 1990). "Evaluation of clinical criteria for cluster headache with special reference to the classification of the International Headache Society". Cephalalgia. 10 (4): 195–7. doi:10.1046/j.1468-2982.1990.1004195.x. PMID 2245469.
  30. ↑ Sandrini G, Antonaci F, Pucci E, Bono G, Nappi G (December 1994). "Comparative study with EMG, pressure algometry and manual palpation in tension-type headache and migraine". Cephalalgia. 14 (6): 451–7, discussion 394–5. doi:10.1046/j.1468-2982.1994.1406451.x. PMID 7697707.
  31. ↑ Jensen R, Fuglsang-Frederiksen A (June 1994). "Quantitative surface EMG of pericranial muscles. Relation to age and sex in a general population". Electroencephalogr Clin Neurophysiol. 93 (3): 175–83. doi:10.1016/0168-5597(94)90038-8. PMID 7515793.
  32. ↑ <ref name="pmid24795685">Bieńkiewicz MM, Brandi ML, Goldenberg G, Hughes CM, Hermsdörfer J (2014). "The tool in the brain: apraxia in ADL. Behavioral and neurological correlates of apraxia in daily living". Front Psychol. 5: 353. doi:10.3389/fpsyg.2014.00353. PMC 4005934. PMID 24795685.
  33. ↑ <ref name="pmid25936541">Civelek GM, Atalay A, Turhan N (2015). "Association of ideomotor apraxia with lesion site, etiology, neglect, and functional independence in patients with first ever stroke". Top Stroke Rehabil. 22 (2): 94–101. doi:10.1179/1074935714Z.0000000027. PMID 25936541.
  34. ↑ <ref name="pmid17507030">Wheaton LA, Hallett M (2007). "Ideomotor apraxia: a review". J Neurol Sci. 260 (1–2): 1–10. doi:10.1016/j.jns.2007.04.014. PMID 17507030.
  35. ↑ <ref name="pmid15509449">McClain M, Foundas A (2004). "Apraxia". Curr Neurol Neurosci Rep. 4 (6): 471–6. doi:10.1007/s11910-004-0071-z. PMID 15509449.
  36. ↑ <ref name="pmid26942323">Frenkel-Toledo S, Liebermann DG, Bentin S, Soroker N (2016). "Dysfunction of the Human Mirror Neuron System in Ideomotor Apraxia: Evidence from Mu Suppression". J Cogn Neurosci. 28 (6): 775–91. doi:10.1162/jocn_a_00936. PMID 26942323.
  37. ↑ <ref name="Hagmann1998">Hagmann, Georg Goldenberg Sonja (1998). "Therapy of Activities of Daily Living in Patients with Apraxia". Neuropsychological Rehabilitation. 8 (2): 123–141. doi:10.1080/713755559. ISSN 0960-2011.
  38. ↑ <ref name="pmid18254038">West C, Bowen A, Hesketh A, Vail A (2008). "Interventions for motor apraxia following stroke". Cochrane Database Syst Rev (1): CD004132. doi:10.1002/14651858.CD004132.pub2. PMC 6464830. PMID 18254038.
  39. ↑ <ref name="van HeugtenDekker2016">van Heugten, C M; Dekker, J; Deelman, B G; van Dijk, A J; Stehmann-Saris, J C (2016). "Outcome of strategy training in stroke patients with apraxia: a phase II study". Clinical Rehabilitation. 12 (4): 294–303. doi:10.1191/026921598674468328. ISSN 0269-2155.
  40. ↑ <ref name="Butler2016">Butler, Jenny (2016). "Intervention Effectiveness: Evidence from a Case Study of Ideomotor and Ideational Apraxia". British Journal of Occupational Therapy. 60 (11): 491–497. doi:10.1177/030802269706001109. ISSN 0308-0226.
  41. ↑ <ref name="pmid2799873">"Stroke--1989. Recommendations on stroke prevention, diagnosis, and therapy. Report of the WHO Task Force on Stroke and other Cerebrovascular Disorders". Stroke. 20 (10): 1407–31. 1989. doi:10.1161/01.str.20.10.1407. PMID 2799873.
  42. ↑ <ref name="pmid26300647">Esenwa C, Gutierrez J (2015). "Secondary stroke prevention: challenges and solutions". Vasc Health Risk Manag. 11: 437–50. doi:10.2147/VHRM.S63791. PMC 4536764. PMID 26300647.
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