Sandbox:nou

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

Symptom or finding	Diagnoses that are suggested by the finding
Altered mental status	Wernicke’s encephalopathy; stroke; encephalitis; seizure; intoxication with alcohol, illicit drugs, carbon monoxide; hypertensive encephalopathy
Transient loss of consciousness	Arrhythmia; acute coronary syndrome; aortic dissection; pulmonary embolism; vasovagal syncope; hypovolemia; stroke; subarachnoid hemorrhage; seizure
Headache	Stroke; craniocervical vascular dissection; meningitis; carbon monoxide exposure; vestibular migraine; high or low intracranial pressure; subarachnoid hemorrhage
Neck pain	Craniocervical vascular dissection (esp. vertebral artery)
Chest/back pain	Acute coronary syndrome; aortic dissection
Abdominal/back pain	Ruptured ectopic pregnancy; aortic dissection
Dyspnea	Pulmonary embolism; pneumonia; anemia
Palpitations	Arrhythmia; vasovagal syncope; panic disorder
Bleeding or fluid losses	Hypovolemia; anemia
New/recent medication use	Medication side effects or toxicity (e.g., gentamicin)
Fever or chills	Systemic infection; encephalitis; mastoiditis; meningitis
Abnormal glucose	Symptomatic hypoglycemia, diabetic ketoacidosis

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

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.

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