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{| class="wikitable"
|+Pathophysiology based on the causes
!Cause
!Pathophysiology
!Catogery of dizziness
|-
|Orthostatic hypotension
|It is a drop in blood pressure on changing the position or can be due to the side effect of the medicine
|Presyncope
|-
|Benign paroxysmal positional vertigo
|The semicircular canal contains loose otolith, which gives a false sense of motion.
|Vertigo
|-
|Meniere disease
|Excessive endolymphatic fluid in the inner ear
|Vertigo
|-
|Hyperventilation syndrome
|Hyperventilation leads to respiratory alkalosis
|Lightheadedness
|-
|Peripheral neuropathy
|Decrease tactile sensation may cause patients to lack the feeling of feet to be touched to the ground leading to falls and imbalance.
|Disequilibrium
|-
|Parkinson disease
|Gait dysfunction cause falls and imbalance
|Disequilibrium
|-
|Vestibular migraine
|Uncertain
|Vertigo
|}
{| class="wikitable"
! colspan="1" rowspan="1" |Symptom or finding
|-
| colspan="1" rowspan="1" |Altered mental status
|-
| colspan="1" rowspan="1" |Transient loss of consciousness
|-
| colspan="1" rowspan="1" |Headache
|-
| colspan="1" rowspan="1" |Neck pain
|-
| colspan="1" rowspan="1" |Chest/back pain
|-
| colspan="1" rowspan="1" |Abdominal/back pain
|-
| colspan="1" rowspan="1" |Dyspnea
|-
| colspan="1" rowspan="1" |Palpitations
|-
| colspan="1" rowspan="1" |Bleeding or fluid losses
|-
| colspan="1" rowspan="1" |New/recent medication use
|-
| colspan="1" rowspan="1" |Fever or chills
|-
| colspan="1" rowspan="1" |Abnormal glucose
|}{{familytree/start}}
{{familytree | | | | | | | | | | | | | | | | A01 | | | | | |A01=Drop of systolic BP > 20 mmHg (30 for hypertensive patients)}}
{{familytree | | | | | | | | | | | | | | | | |!| | | | | | | | }}
{{familytree | | | | | | | | | |,|-|-|-|-|-|-|^|-|-|-|-|-|-|.| }}
{{familytree | | | | | | | | | C01 | | | | | | | | | | | |C02|C01=Symptomatic|C02=Asymptomatic}}
{{familytree | | | | | | | | | |!| | | | | | | | | | | | | |!| }}
{{familytree | | | | | | | | | D01 | | | | | | | | | | | |D02|D01=Non-pharmacological treatment|D02=Observation
and follow-up}}
{{familytree | | | | | | | | | |!| | | | | | | | | }}
{{familytree | | | | | | | | | E01 | | | | | | | |E01=Persistance of symtoms}}
{{familytree | | | | | | | | | |!| | | | | | | | | }}
{{familytree | | | | | | | | | E01 | | | | | | | |E01=Pharmacological Treatment}}
{{familytree | | | | | | | | | |!| | | | | | | | | }}
{{familytree | | |,|-|-|-|-|-|-|^|-|-|-|-|-|-|.| | }}
{{familytree | | |!| | | | | | | | | | | | | |!| | }}
{{familytree | | E01 | | | | | | | | | | | | E02 | | |E01=No supine hypertension or chronic heart failure|E02=Supine hypertension or chronic heart failure: }}
{{familytree | | |!| | | | | | | | | | | | | |!| | }}
{{familytree | | E01 | | | | | | | | | | | | E02 | | E01= Fludrocortisone<br>Midodrine|E02=Midodrine}}
{{familytree/end}}<br />
{| class="wikitable"
|+
!Non- pharmacological therapy
!Surgical Treatment
|'''Alternative treatments'''
|-
|Cognitive Behavioral Therapy
|Round window reinforcement
|Excercise, yoga,meditation
|-
|Tinnitus retraining therapy (TRT)
|Oval window reinforcement
|Massage,relaxing therapy,hypnosis
|-
|Directive Counselling
|
|Vitamin and supplements
|}
Dr Norina Usma
Dr Norina Usma


_NOTOC_
_NOTOC_
===Differentiating [disease name] from other diseases on the basis of [symptom 1], [symptom 2], and [symptom 3]===
On the basis sign and symptoms hyperacusis must be differentiated from misphonia, phonophobia, tinnitus, william syndrome,lyme disease,migraine .
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Diseases
| colspan="6" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Clinical manifestations'''
! rowspan="2" |Para-clinical findings
| colspan="1" rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Gold standard'''
|-
| colspan="3" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Symptoms'''
! colspan="3" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical examination
|-
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |
|-
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Negative emotional reaction
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Ringing in the ears
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Psychiatric disorders
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Hearing loss
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Sound sensitivity
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Loudness discomfort level
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Misphonia
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |Limbic system involved
| style="background: #F5F5F5; padding: 5px;" |Clinical diagnosis
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Phonophobia
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |Limbic system involved
| style="background: #F5F5F5; padding: 5px;" |Clinical diagnosis
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Tinnitus
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |8th cranial nerve palsy/ auditory system involved
| style="background: #F5F5F5; padding: 5px;" |Audiological exam
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |William Syndrome
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |Genetic disorder
| style="background: #F5F5F5; padding: 5px;" |Micro-array analysis/FISH and audiological exam
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Lyme Disease
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |Auditory system involved
| style="background: #F5F5F5; padding: 5px;" |Audiological exam
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Migraine
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" |Trigeminal ganglion stimulation
| style="background: #F5F5F5; padding: 5px;" |Clinical diagnosis
|}
==References==
{{Reflist|2}}{{WH}}{{WS}}




== Historical Perspective==
== What are the Symptoms of Apraxia?==
Symptoms of apraxia of speech include:


* Repeated, distorted, or left outspoken words.
'''Initial orthostatic hypotension (iOH)'''
* Struggling to speak the right word
* More trouble using longer terms, either some time or all the time
* Poor speaking ability


==What Causes Apraxia?==
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.
Damage to brain can lead to apraxia When apraxia progresses in a person who was before able to perform the abilities or task, it is termed as acquired apraxia.


The most common causes of apraxia are:
'''Neurogenic orthostatic hypotension (nOH)'''


* Neurodegenerative illness
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.
* Brain tumor
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.
* Dementia
* Stroke
'''Delayed orthostatic hypotension (dOH)'''
* Traumatic brain injury


==Who is at Highest Risk?==
Delayed orthostatic hypotension (dOH) is demarcated as a fall in blood pressure that accomplishes neurogenic orthostatic hypotension criteria but ensues after three minutes.  
Stroke is the most common cause of apraxia, which is more common in older adults. The factors that increase the risk of apraxia are the same as a stroke, such as high blood pressure, high cholesterol, prior stroke, and transient ischemic stroke.


==Diagnosis==
'''Neurally mediated syncope (vOH)'''
The following test should be done if the cause is unknown:


* MRI or CT scans of the brain to rule out stroke, tumor or another brain injury
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.  
* An EEG electroencephalogram to find out other causes of apraxia.
* Spinal tap to check for inflammation.


==When to Seek Urgent Medical Care?==
'''Cardiovascular orthostatic hypotension (cOH)'''
The patient needs to contact the doctor if he/she has symptoms of apraxia or difficulty accomplishing everyday tasks after a brain injury or stroke.


==Treatment Options==
Cardiovascular orthostatic hypotension occurs from intravascular hypovolemia or reduced cardiac output along with compensatory tachycardia.
Treatment depends on what type of apraxia a person is having. Following are the treatment programs:


* Speech Therapy
'''Orthostatic pseudohypotension (pOH)'''
* Physical therapy
* Occupational therapy
* Cognitive rehabilitation


==Where to find Medical Care for (Disease name)?==
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.
Medical care for (disease name) can be found [https://www.google.com/maps/search/hospitals/ here].
==Prevention==
Decreasing the risk of brain injury and stroke may help prevent circumstances that cause apraxia.


==What to Expect (Outlook/Prognosis)?==
==Pathophysiology==
Patients with apraxia are not able to do things independently and may distress carrying out everyday responsibilities. Activities should be avoided that can lead to injury and take the appropriate safety actions.


== Possible Complications==
*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.
Apraxia may cause:
*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.


* Learning problems
==Causes==
* Low self-esteem
* Social problems


== Sources<ref><nowiki><ref name="pmid26281194"></nowiki>{{cite journal| author=Krasnova TN, Samokhodskaya LM, Ivanitsky LV, Korogodina AD, Borisov EN, Nikiforova NV | display-authors=etal| title=[Impact of interleukin-10 and interleukin-28 gene polymorphisms on the development and course of lupus nephritis]. | journal=Ter Arkh | year= 2015 | volume= 87 | issue= 6 | pages= 40-44 | pmid=26281194 | doi=10.17116/terarkh201587640-44 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26281194  }}</ref>==
'''Primary:'''
<br />
==Classification==
Apraxia may be classified into different subtypes based on it's clinical features:


*'''Ideomotor apraxia''': The most commonly known type of apraxia is Ideomotor apraxia, or decreased performance of skilled motor performances despite integral language, sensory and motor function<ref><nowiki><ref name="pmid1115438"></nowiki>{{cite journal| author=Geschwind N| title=The apraxias: neural mechanisms of disorders of learned movement. | journal=Am Sci | year= 1975 | volume= 63 | issue= 2 | pages= 188-95 | pmid=1115438 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1115438  }}</ref>. Ideomotor apraxia is classically demonstrated when a patient questioned verbally to make a motion with a limb. Patients with Ideomotor apraxia display spatial and temporal errors, inconvenient timing, amplitude, sequencing, configuration,  limb position in space.  It is an inability to carry out, learned motor acts, command, adequate motor, and sensory abilities. Ideomotor apraxia can be due to cerebral damage in numerous areas, including the left parietal lobe, the intrahemispheric association fibers, the dominant hemisphere motor association cortex, and the anterior corpus callosum. In the last two, ideomotor apraxia is usually restricted to the left arm. They often use their arm as an object relatively than indicating how to use the object . Patients are frequently able to achieve the same acts without struggle in their daily lives. This process has been called the "voluntary-automatic dissociation"<ref>Schnider A, Hanlon RE, Alexander DN, Benson DF. [https://doi.org/10.1006/brln.1997.1770 Ideomotor apraxia: behavioral dimensions and neuroanatomical basis.] ''Brain Lang''. 1997;58(1):125-136. doi:10.1006/brln.1997.1770</ref><ref><nowiki><ref name="pmid8292325"></nowiki>{{cite journal| author=Rapcsak SZ, Ochipa C, Beeson PM, Rubens AB| title=Praxis and the right hemisphere. | journal=Brain Cogn | year= 1993 | volume= 23 | issue= 2 | pages= 181-202 | pmid=8292325 | doi=10.1006/brcg.1993.1054 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8292325  }}</ref>.These patients have a deficiency in their skill to plan or ample motor actions that depend on semantic memory. They can describe how to achieve a response, but incapable to "imagine" or do the movement. Though the capability to perform an act inevitably when cued remains complete, this is recognized as automatic-voluntary dissociation<ref><nowiki><ref name="pmid82923253"></nowiki>{{cite journal| author=Rapcsak SZ, Ochipa C, Beeson PM, Rubens AB| title=Praxis and the right hemisphere. | journal=Brain Cogn | year= 1993 | volume= 23 | issue= 2 | pages= 181-202 | pmid=8292325 | doi=10.1006/brcg.1993.1054 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8292325  }}</ref>.
*Parkinson disease
*'''Constructional apraxia:'''  It is a condition resulting from neurological damage, which is demonstrated by the inability to construct and copy to command two- and three-dimensional stimuli. Constructional apraxia has been a classic sign of a parietal lobe lesion, and as a valuable tool to escalate the spatial abilities functioned by this lobe. It has become gradually clear that Constructional Apraxia is a complex construct that can be observed with very different tasks that are only slightly interrelated, and hit various kinds of visuospatial, attentional, perceptual, planning, and motor mechanisms<ref><nowiki><ref name="pmid8174333"></nowiki>{{cite journal| author=Yanagisawa N, Ueno E, Hayashi R, Tokuda T, Takou K| title=[Apraxia of gait and disorders in posture and locomotion]. | journal=Rinsho Shinkeigaku | year= 1993 | volume= 33 | issue= 12 | pages= 1310-2 | pmid=8174333 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174333  }}</ref>.The patient with constructional apraxia is unable to construct, draw, or copy simple configurations; for example, intersecting shapes; they have trouble drawing basic shapes or copying a simple diagram<ref><nowiki><ref name="pmidhttps://doi.org/10.1016/S0010-9452(64)80020-4"></nowiki>{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://doi.org/10.1016/S0010-9452(64)80020-4 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10  }}</ref>.
*Pure autonomic failure
*'''Buccofacial or orofacial apraxia:''' This is the most common type of apraxia; patients cannot convey facial movements on requests, such as voluntary movements of the tongue, cheeks, lips, pharynx, or larynx on command, for example, include licking lips, whistling, coughing, or winking)<ref><nowiki><ref name="pmid30311153"></nowiki>{{cite journal| author=Khalili M, Wong RJ| title=Underserved Does Not Mean Undeserved: Unfurling the HCV Care in the Safety Net. | journal=Dig Dis Sci | year= 2018 | volume= 63 | issue= 12 | pages= 3250-3252 | pmid=30311153 | doi=10.1007/s10620-018-5316-9 | pmc=6436636 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30311153  }}</ref></ref>.
*Multiple system atrophy
*'''Gait apraxia:''' Apraxia of gait is a rare locomotion syndrome categorized by the incapability of lifting the feet from the floor regardless of discontinuous stepping action. The accountable site of lesions is in the basal ganglia and frontal lobe<ref><nowiki><ref name="pmid8174333"></nowiki>{{cite journal| author=Yanagisawa N, Ueno E, Hayashi R, Tokuda T, Takou K| title=[Apraxia of gait and disorders in posture and locomotion]. | journal=Rinsho Shinkeigaku | year= 1993 | volume= 33 | issue= 12 | pages= 1310-2 | pmid=8174333 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174333  }}</ref></ref>'''.'''
*Autoimmune autonomic gangliopathy
*'''Limb-kinetic apraxia:''' It is the failure to make precise movements with an arm, finger, or leg. For example, a person may have trouble tying their shoes, waving hello, or typing on a computer.
*Lewy body dementia
*Rare Hereditary disorders (Familial dysautonomia, dopamine beta hydrolase deficiency)


==Pathophysiology==
'''Secondary:'''


* Ideational apraxia patients may be diminished in sequencing a sequence of acts, or make contented errors, also stated to as `conceptual apraxia' by some investigators<ref><nowiki><ref name="pmid3179688"></nowiki>{{cite journal| author=De Renzi E, Lucchelli F| title=Ideational apraxia. | journal=Brain | year= 1988 | volume= 111 ( Pt 5) | issue=  | pages= 1173-85 | pmid=3179688 | doi=10.1093/brain/111.5.1173 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3179688  }}</ref><nowiki></ref></nowiki>.
*Iatrogenic (drug-related,
* Patients with ideomotor apraxia (IMA) make temporal and spatial errors discrete to the primary motor deficit, whereas patients with limb-kinetic apraxia present with elemental motor deficits such as loss of independent finger movements and slow-stiff movements in the absence of weakness.
*Diabetes mellitus
* Ideomotor apraxia causes the damage of either the corticocortical connecting pathways or the dominant cerebral cortex in the perirolandic or suprasylvian region of the left dominant hemisphere.
*Alcoholic polyneuropathy
** However, to detect one specific cortical locus, when this pathology induces IMA, it recommends that a distributed modular system intermediates praxis<ref><nowiki><ref name="pmid17507030"></nowiki>{{cite journal| author=Wheaton LA, Hallett M| title=Ideomotor apraxia: a review. | journal=J Neurol Sci | year= 2007 | volume= 260 | issue= 1-2 | pages= 1-10 | pmid=17507030 | doi=10.1016/j.jns.2007.04.014 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17507030  }}</ref><nowiki></ref></nowiki>.
*Amyloidosis
* Major strokes involving the middle cerebral artery not only extend outside specific cortical areas but often extend subcortically to periventricular white matter and basal ganglia structures.
*Multiple myeloma
* Due to infarction, there can be areas of decreased blood flow which are inadequate to cause cystic infarction but are enough to cause ischaemic neuronal damage.
*Endocrine Disease (adrenal insufficiency, thyroid disease, diabetes insipidus)
* Infarctions restricted to the basal ganglia are not common, and other structures such as the insula, thalamus, and surrounding white matter are often involved.
*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


<br />
==Differentiating Xyz from Other Diseases==


==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.
'''Intravascular volume depletion''':
*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.
Blood loss
* 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><nowiki><ref name="pmid15509449"></nowiki>{{cite journal| author=McClain M, Foundas A| title=Apraxia. | journal=Curr Neurol Neurosci Rep | year= 2004 | volume= 4 | issue= 6 | pages= 471-6 | pmid=15509449 | doi=10.1007/s11910-004-0071-z | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15509449  }}</ref><nowiki></ref></nowiki>.
Dehydration
* Patients with apraxia cannot regain these representations of stored, skilled actions.Therefore, patients with apraxia are unable to perform daily living activities well.
Pregnancy/postpartum
Shock


==Differentiating Xyz from Other Diseases==
'''Cardiovascular''':
==Epidemiology and Demographics==
Anemia
'''Incidence'''
Cardiac arrhythmia
Congestive heart failure
Myocardial infarction
Myocarditis
Pericarditis
Valvular heart disease
Venous insufficiency
Postprandial hypotension


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<ref><nowiki><ref name="pmid10768524"></nowiki>{{cite journal| author=Smania N, Girardi F, Domenicali C, Lora E, Aglioti S| title=The rehabilitation of limb apraxia: a study in left-brain-damaged patients. | journal=Arch Phys Med Rehabil | year= 2000 | volume= 81 | issue= 4 | pages= 379-88 | pmid=10768524 | doi=10.1053/mr.2000.6921 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10768524  }}</ref>.
'''Neurologic Causes''':
Amyloidosis (hereditary and primary)
Diabetic autonomic neuropathy
Lewy body dementia
Multisystem atrophy (Shy-Drager syndrome)
Parkinson disease
Pure autonomic failure


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


Prevalence rates of  apraxia range among 0 and 34% for patients with Right hemisphere stroke and 28–57% for patients with Left hemisphere stroke<ref><nowiki><ref name="pmid31002018"></nowiki>{{cite journal| author=Buchmann I, Dangel M, Finkel L, Jung R, Makhkamova I, Binder A | display-authors=etal| title=[Formula: see text] Limb apraxia profiles in different clinical samples. | journal=Clin Neuropsychol | year= 2020 | volume= 34 | issue= 1 | pages= 217-242 | pmid=31002018 | doi=10.1080/13854046.2019.1585575 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31002018  }}</ref>.Real tool-use loss prevalence rates were stated with 25–54% impaired level of patients
'''Endocrine Causes''':
Adrenal insufficiency
Diabetes insipidus
Hyperglycemia, acute
Hypoaldosteronism
Hypokalemia
Hypothyroidism
Pheochromocytoma


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


Apraxia commonly affects individuals older than 50 years of age.
==Epidemiology and Demographics==
 
<br />
'''Gender'''  
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Headache]]
 
'''For the WikiDoc page for this topic, click [[Headache|here]]'''
Apraxia affects men and women equally.
{{CMG}} {{AE}} {{SAI}}


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.


==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<ref><nowiki><ref name="pmid18957186"></nowiki>{{cite journal| author=Gross RG, Grossman M| title=Update on apraxia. | journal=Curr Neurol Neurosci Rep | year= 2008 | volume= 8 | issue= 6 | pages= 490-6 | pmid=18957186 | doi=10.1007/s11910-008-0078-y | pmc=2696397 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18957186  }}</ref>. Risk factors for apraxia are similar as risk factors of stroke which include


* High blood pressure
{| class="wikitable"
* High cholesterol
|+
* Diabetes
! rowspan="2" |Disease
* Smoking
! colspan="4" |History and Physical Examination
* Prior stroke or cardiovascular disease
!
* Prior transient ischemic attack (TIA)
! colspan="3" |Diagnostic approach
* Dialysis treatment
|-
!Proteinuria
!Hematuria
!Peripheral edema
!Hypertension
!Weight gain
!C4 dense deposition in the glomerulus
!Complement pathway
!Gold standard test
|-
|[[Migraine|'''IgA Nephropathy''']]
| +
| +
| +
| +
| +
|Mesengial
| -
|Renal biopsy
|-
|[[Tension-type headache|'''Membranous Nephropathy''']]
|<nowiki>+</nowiki>
| -
| +
|<nowiki>-</nowiki>
| +
|Glomerular capillary wall
| -
|Renal biopsy
|-
|[[Cluster headache|'''''Focal Segmental Glomerulus /Minimal Change Disease''''']]
| +
| +
| +
|<nowiki>-</nowiki>
| +
|No Cd4 deposits
| +
|Renal biopsy
|-
|[[Seizure|'''Membranoproliferative glomerulonephritis''']]
|<nowiki>+</nowiki>
|<nowiki>-</nowiki>
| +
| +
| +
|Along capillary walls
| -
|Renal biopsy
|-
|[[Meningitis|'''Lupus Nephritis''']]
| -
| +
| +
| +
| +
|Mesangium and capillary wall
| +
|Renal biopsy
|}


==Screening==
==Screening==
Line 127: Line 383:
==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==


* The symptoms of apraxia typically develop during early or later years depending on the cause and the location affected.
*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<ref><nowiki><ref name="pmid24795685"></nowiki>{{cite journal| author=Bieńkiewicz MM, Brandi ML, Goldenberg G, Hughes CM, Hermsdörfer J| title=The tool in the brain: apraxia in ADL. Behavioral and neurological correlates of apraxia in daily living. | journal=Front Psychol | year= 2014 | volume= 5 | issue=  | pages= 353 | pmid=24795685 | doi=10.3389/fpsyg.2014.00353 | pmc=4005934 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24795685  }}</ref>.
*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 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.  
*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.
*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.
*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 ====
====Complications====
Common complications of apraxia include:
Common complications of apraxia include:


* Broca's Aphasia
*Broca's Aphasia
* Acalculi
*Acalculi
* Right-left Confusion
*Right-left Confusion
* Alexia with agraphia
*Alexia with agraphia
* Wernicke's Aphasia.
*Wernicke's Aphasia.
 
====Prognosis====


==== 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.<br />


* 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<ref><nowiki><ref name="pmid25936541"></nowiki>{{cite journal| author=Civelek GM, Atalay A, Turhan N| title=Association of ideomotor apraxia with lesion site, etiology, neglect, and functional independence in patients with first ever stroke. | journal=Top Stroke Rehabil | year= 2015 | volume= 22 | issue= 2 | pages= 94-101 | pmid=25936541 | doi=10.1179/1074935714Z.0000000027 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25936541  }}</ref>.
* 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.<br />
===Diagnostic Study of Choice===
===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.  
*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.
*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.
*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<ref><nowiki><ref name="pmid17507030"></nowiki>{{cite journal| author=Wheaton LA, Hallett M| title=Ideomotor apraxia: a review. | journal=J Neurol Sci | year= 2007 | volume= 260 | issue= 1-2 | pages= 1-10 | pmid=17507030 | doi=10.1016/j.jns.2007.04.014 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17507030  }}</ref>.
*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 <ref><nowiki><ref name="pmid15509449"></nowiki>{{cite journal| author=McClain M, Foundas A| title=Apraxia. | journal=Curr Neurol Neurosci Rep | year= 2004 | volume= 4 | issue= 6 | pages= 471-6 | pmid=15509449 | doi=10.1007/s11910-004-0071-z | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15509449  }}</ref>. Apraxia should not be mixed up with aphasia (the inability to understand language); though, they often occur together.
*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===
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.
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: =====
=====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.  
*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.  
*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.  
*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.  
*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.  
*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<ref><nowiki><ref name="pmid26942323"></nowiki>{{cite journal| author=Frenkel-Toledo S, Liebermann DG, Bentin S, Soroker N| title=Dysfunction of the Human Mirror Neuron System in Ideomotor Apraxia: Evidence from Mu Suppression. | journal=J Cogn Neurosci | year= 2016 | volume= 28 | issue= 6 | pages= 775-91 | pmid=26942323 | doi=10.1162/jocn_a_00936 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26942323  }}</ref>.
*The response is recorded as an error.


===== Buccofacial apraxia: =====
=====Buccofacial apraxia:=====


* Patients cannot do skilled actions.
*Patients cannot do skilled actions.


===== Constructional apraxia: =====
=====Constructional apraxia:=====


* Failure to copy or draw quality images.  
*Failure to copy or draw quality images.
* Localizes lesions involving frontal or parietal area.<ref><nowiki><ref name="pmid1995-97708-000"></nowiki>{{cite journal| author=Odelola HA, Koza J| title=Characterization of Nigerian strains of West Nile virus by plaque formation. | journal=Acta Virol | year= 1975 | volume= 19 | issue= 6 | pages= 489-92 | pmid=1995-97708-000 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1995  }}</ref>
*Localizes lesions involving frontal or parietal area.


===Laboratory Findings===
===Laboratory Findings===
Line 195: Line 452:
Brain CT scan may be helpful in the diagnosis of Apraxia. Findings on CT scan suggestive of/diagnostic of Apraxia include  
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 look for a mass lesion and
* To evaluate for possible atrophy expressive of a degenerative condition.
*To evaluate for possible atrophy expressive of a degenerative condition.


===MRI===
===MRI===
Line 214: Line 471:
There are no specific recommended therapeutic interventions for the management of Apraxia.
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<ref><nowiki><ref name="Hagmann1998"></nowiki>{{cite journal|last1=Hagmann|first1=Georg Goldenberg Sonja|title=Therapy of Activities of Daily Living in Patients with Apraxia|journal=Neuropsychological Rehabilitation|volume=8|issue=2|year=1998|pages=123–141|issn=0960-2011|doi=10.1080/713755559}}</ref>. There are limited information and research available regarding various treatments<ref><nowiki><ref name="pmid18254038"></nowiki>{{cite journal| author=West C, Bowen A, Hesketh A, Vail A| title=Interventions for motor apraxia following stroke. | journal=Cochrane Database Syst Rev | year= 2008 | volume=  | issue= 1 | pages= CD004132 | pmid=18254038 | doi=10.1002/14651858.CD004132.pub2 | pmc=6464830 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18254038  }}</ref></ref>. Various interventions include:
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<nowiki></ref></nowiki>. Various interventions include:


* Daily living doings training: this method explains internal and external compensatory approaches that permit a functional mission to be accomplished<ref><nowiki><ref name="van HeugtenDekker2016"></nowiki>{{cite journal|last1=van Heugten|first1=C M|last2=Dekker|first2=J|last3=Deelman|first3=B G|last4=van Dijk|first4=A J|last5=Stehmann-Saris|first5=J C|title=Outcome of strategy training in stroke patients with apraxia: a phase II study|journal=Clinical Rehabilitation|volume=12|issue=4|year=2016|pages=294–303|issn=0269-2155|doi=10.1191/026921598674468328}}</ref>.
*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<ref><nowiki><ref name="Butler2016"></nowiki>{{cite journal|last1=Butler|first1=Jenny|title=Intervention Effectiveness: Evidence from a Case Study of Ideomotor and Ideational Apraxia|journal=British Journal of Occupational Therapy|volume=60|issue=11|year=2016|pages=491–497|issn=0308-0226|doi=10.1177/030802269706001109}}</ref>.
*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;
*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;
*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;
*Cueing, physical or verbal stimuli: This technique enables each phase of the task to be completed;


===Surgery===
===Surgery===
Line 226: Line 483:


===Primary Prevention===
===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<ref><nowiki><ref name="pmid2799873"></nowiki>{{cite journal| author=| title=Stroke--1989. Recommendations on stroke prevention, diagnosis, and therapy. Report of the WHO Task Force on Stroke and other Cerebrovascular Disorders. | journal=Stroke | year= 1989 | volume= 20 | issue= 10 | pages= 1407-31 | pmid=2799873 | doi=10.1161/01.str.20.10.1407 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2799873  }}</ref>. Some steps include:
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.
*Exercise regularly.
* Eat a healthy diet.
*Eat a healthy diet.
* Limit how much alcohol you drink.
*Limit how much alcohol you drink.
* Quit smoking
*Quit smoking
* Check your blood pressure often.
*Check your blood pressure often.


===Secondary Prevention===
===Secondary Prevention===
Secondary prevention of stroke is the mainstay of preventing Apraxia as it is the leading cause of the various type of Apraxia<ref><nowiki><ref name="pmid26300647"></nowiki>{{cite journal| author=Esenwa C, Gutierrez J| title=Secondary stroke prevention: challenges and solutions. | journal=Vasc Health Risk Manag | year= 2015 | volume= 11 | issue=  | pages= 437-50 | pmid=26300647 | doi=10.2147/VHRM.S63791 | pmc=4536764 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26300647  }}</ref>. Effective measures for the secondary prevention of Apraxia include:
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  
*Aspirin, clopidogrel, extended-release dipyridamole, ticlopidine
* Anticoagulants (apixaban, dabigatran, edoxaban, rivaroxaban, warfarin)
*Anticoagulants (apixaban, dabigatran, edoxaban, rivaroxaban, warfarin)
* Blood pressure-lowering medications.
*Blood pressure-lowering medications.
* Diabetes Control
*Diabetes Control
* Low-fat diet
*Low-fat diet
* Cholesterol-lowering medications, Cessation of cigarette smoking, carotid revascularization
*Cholesterol-lowering medications, Cessation of cigarette smoking, carotid revascularization


* Weight loss and Exercise
*Weight loss and Exercise


==References==
==References==
{{reflist|2}}
{{reflist|2}}
<references />

Latest revision as of 04:59, 29 August 2020

Pathophysiology based on the causes
Cause Pathophysiology Catogery of dizziness
Orthostatic hypotension It is a drop in blood pressure on changing the position or can be due to the side effect of the medicine Presyncope
Benign paroxysmal positional vertigo The semicircular canal contains loose otolith, which gives a false sense of motion. Vertigo
Meniere disease Excessive endolymphatic fluid in the inner ear Vertigo
Hyperventilation syndrome Hyperventilation leads to respiratory alkalosis Lightheadedness
Peripheral neuropathy Decrease tactile sensation may cause patients to lack the feeling of feet to be touched to the ground leading to falls and imbalance. Disequilibrium
Parkinson disease Gait dysfunction cause falls and imbalance Disequilibrium
Vestibular migraine Uncertain Vertigo
Symptom or finding
Altered mental status
Transient loss of consciousness
Headache
Neck pain
Chest/back pain
Abdominal/back pain
Dyspnea
Palpitations
Bleeding or fluid losses
New/recent medication use
Fever or chills
Abnormal glucose
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Drop of systolic BP > 20 mmHg (30 for hypertensive patients)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Symptomatic
 
 
 
 
 
 
 
 
 
 
 
Asymptomatic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Non-pharmacological treatment
 
 
 
 
 
 
 
 
 
 
 
Observation and follow-up
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Persistance of symtoms
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pharmacological Treatment
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
No supine hypertension or chronic heart failure
 
 
 
 
 
 
 
 
 
 
 
Supine hypertension or chronic heart failure:
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Fludrocortisone
Midodrine
 
 
 
 
 
 
 
 
 
 
 
Midodrine
 


Non- pharmacological therapy Surgical Treatment Alternative treatments
Cognitive Behavioral Therapy Round window reinforcement Excercise, yoga,meditation
Tinnitus retraining therapy (TRT) Oval window reinforcement Massage,relaxing therapy,hypnosis
Directive Counselling Vitamin and supplements

Dr Norina Usma

_NOTOC_

Differentiating [disease name] from other diseases on the basis of [symptom 1], [symptom 2], and [symptom 3]

On the basis sign and symptoms hyperacusis must be differentiated from misphonia, phonophobia, tinnitus, william syndrome,lyme disease,migraine .

Diseases Clinical manifestations Para-clinical findings Gold standard
Symptoms Physical examination
Negative emotional reaction Ringing in the ears Psychiatric disorders Hearing loss Sound sensitivity Loudness discomfort level
Misphonia + - + +/- - - Limbic system involved Clinical diagnosis
Phonophobia + - + +/- - - Limbic system involved Clinical diagnosis
Tinnitus +/- + + - + + 8th cranial nerve palsy/ auditory system involved Audiological exam
William Syndrome +/- - +/- + + + Genetic disorder Micro-array analysis/FISH and audiological exam
Lyme Disease + + +/- + + + Auditory system involved Audiological exam
Migraine - + - - + +/- Trigeminal ganglion stimulation Clinical diagnosis

References

Template:WHTemplate:WS


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

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.


Disease History and Physical Examination Diagnostic approach
Proteinuria Hematuria Peripheral edema Hypertension Weight gain C4 dense deposition in the glomerulus Complement pathway Gold standard test
IgA Nephropathy + + + + + Mesengial - Renal biopsy
Membranous Nephropathy + - + - + Glomerular capillary wall - Renal biopsy
Focal Segmental Glomerulus /Minimal Change Disease + + + - + No Cd4 deposits + Renal biopsy
Membranoproliferative glomerulonephritis + - + + + Along capillary walls - Renal biopsy
Lupus Nephritis - + + + + Mesangium and capillary wall + Renal biopsy

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.

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. 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

References