Disorders of autonomic Nervous system for Physiotherapy students

Disorders of Autonomic Nervous system are important for management of patients for physiotherapy rehabilitation. Autonomic Dysreflexia and Horner's syndrome are important for Physiotherapy rehabilitation

1. Disorders of ANS Dr Ira Indurkar MPTh ( Neuro ) Associate professor , Datta M eghe college of physiotherapy

2. Learning Objective At the end the learners will know the important disorders of ANS important for physiotherapy rehabilitation At the students will know the clinical features and management of ANS disorders

3. Introduction to the Autonomic Nervous System (ANS) Autonomic Nervous System (ANS): Part of the peripheral nervous system ;physiological functions ,heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. Two main components of the ANS: Sympathetic nervous system , stimulates the body’s fight-or-flight response Parasympathetic nervous system , which activates the rest and digest or feed and breed responses.

4. Overview of Autonomic Nervous System Disorders  Autonomic Nervous System Disorders as conditions where the ANS fails to work correctly, leading to problems with blood pressure regulation, heart rate, body temperature control, and other bodily functions. • Affects Patient’s quality of life

5. Types of Autonomic Disorders Primary and Secondary Autonomic Disorders. Primary disorders are those where the autonomic nervous system dysfunction is the main characteristic. Examples of primary disorders include Pure Autonomic Failure (PAF), Multiple System Atrophy (MSA), and Familial Dysautonomia Secondary disorders have autonomic dysfunction due to other diseases. Secondary disorders may result from diabetes, Parkinson’s disease, or autoimmune diseases.eg Horner’s syndrome, Autonomic dysreflexia .

6. Causes for Autonomic Nervous System  Causes for Autonomic Nervous System Genetic predispositions, autoimmune diseases, and direct injury to the nerves from trauma or surgery. Diabetes or Parkinson’s can lead to secondary autonomic disorders through the gradual damage of autonomic nerves.

7. Common symptoms of ANS Orthostatic hypotension, abnormal heart rate (either too fast or too slow), digestive issues leading to nausea, bloating, or constipation, and difficulties with the regulation of body temperature.

8. Diagnosing Autonomic Disorders Comprehensive medical history and physical examination. • Specific Tests: tilt table test for diagnosing orthostatic hypotension, Sweat tests for assessing sweat production, Autonomic reflex screening to measure how the autonomic nerve fibers work.

9. Treatments can manage symptoms and improve quality of life. • Treatment options, including medication (e.g., midodrine or fludrocortisone for blood pressure issues), lifestyle changes (increased salt intake, wearing compression stockings), Specific interventions for underlying conditions.

10. Autonomic Dysreflexia Autonomic Dysreflexia is a severe and acute condition characterized by a sudden and excessive uncontrolled sympathetic nervous system response in individuals with spinal cord injuries, typically at or above the T6 level. Understanding AD is vital for physiotherapists, as it requires immediate recognition and management to prevent life-threatening hypertensive emergencies and ensure the safety of patients with spinal cord injuries during rehabilitation.

11. Pathophysiology of Autonomic Dysreflexia  AD occurs when a noxious stimulus below the level of the spinal cord injury triggers an exaggerated sympathetic response. The spinal cord injury prevents the brain from modulating this response, leading to severe hypertension. .

12. Causes and triggers Bladder distension, bowel impaction, skin irritation, or any noxious stimulus below the level of injury Tight clothing, urinary tract infections, or pressure ulcers.

13. Signs and Symptoms Sudden and severe hypertension, pounding headache, flushed face, sweating above the level of injury, nasal congestion, and sometimes blurred vision or feelings of apprehension. Why it is important to identify ?

14. Diagnosis of Autonomic Dysreflexia AD is primarily clinical, based on the sudden onset of symptoms and the presence of a known risk factor (i.e., spinal cord injury at or above T6).

15.  Management and Immediate Care Sit the patient upright (unless contraindicated), remove the triggering stimulus (e.g., emptying the bladder, relieving constipation), and monitor blood pressure closely. • Medical Interventions:Potential need for antihypertensive medications if initial steps do not resolve the hypertension, interdisciplinary approach to managing AD.

16. Physiotherapist’s Role in Management Physiotherapists play a crucial role in educating patients and caregivers about AD, including its triggers and prevention strategies.  Tailored rehabilitation program that considers the risk of AD, including exercises and activities designed to maintain health without overstimulation Long-term Strategies and Patient Education

17. Horner’s Syndrome A condition characterized by a triad of symptoms: Ptosis (drooping of the upper eyelid), Miosis (constricted pupil), and Anhidrosis (absence of sweating) on the affected side of the face.

18. Anatomy and Physiology The three-neuron oculosympathetic pathway is involved in the sympathetic innervation of the eye and surrounding facial structures, and it plays a crucial role in the pathophysiology of Horner’s Syndrome. This pathway comprises three sets of neurons that work in sequence from the hypothalamus to the eye:

19. First-Order Neuron (Central Neuron) • Origin: The first-order neuron begins in the hypothalamus. • Pathway: It descends through the brainstem and cervical spinal cord, specifically down to the C8-T2 level ( ciliospinal center of Budge). • Function: This neuron is responsible for the initial transmission of sympathetic impulses from the brain down to the upper thoracic spine. • Clinical Relevance: Lesions affecting the first-order neuron can result from stroke, multiple sclerosis, or spinal cord injury, leading to a central form of Horner’s Syndrome

20. Second-Order Neuron (Preganglionic Neuron) • Origin: The second-order neuron starts at the ciliospinal center of Budge in the spinal cord (C8-T2 level). • Pathway: It exits the spinal cord and travels over the apex of the lung and into the neck, where it synapses at the superior cervical ganglion located at the level of C2-C4. • Function: This neuron transmits impulses from the spinal cord to the superior cervical ganglion. • Clinical Relevance: Damage to the preganglionic neuron can occur due to lung apex tumors ( Pancoast tumor ), thoracic aortic aneurysms, or traumatic injury to the neck or chest, causing a preganglionic form of Horner’s Syndrome

21. hird -Order Neuron (Postganglionic Neuron) • Origin: The third-order neuron originates in the superior cervical ganglion. • Pathway: After synapsing in the superior cervical ganglion, the postganglionic fibers ascend along the internal carotid artery, without synapsing again, into the skull and innervate the pupil (pupillary dilator muscle), the smooth muscle of the eyelids (Müller’s muscle), and the sweat glands of the forehead and face. • Function: It completes the sympathetic pathway to the eye and upper face, responsible for pupil dilation, eyelid retraction, and facial sweating. • Clinical Relevance: Injuries to the postganglionic neuron, such as carotid artery dissection, skull base fractures, or surgeries that affect the carotid sheath, can lead to a postganglionic form of Horner’s Syndrome.

22. Clinical features  Classic triad of Horner’s Syndrome (ptosis, miosis , anhidrosis ) • Associated Symptoms: Other possible signs like enophthalmos (slight sinking of the eyeball into the orbit) and heterochromia ( color difference in the irises) in congenital cases.

23. Causes of Horner’s Syndrome • Classification of Causes: central, pre-ganglionic, and post-ganglionic, examples of each, stroke for central, chest tumor for pre-ganglionic, and neck trauma for post-ganglionic.

24. Diagnosis of Horner’s Syndrome Clinical examination, including observation of the symptomatic triad. • Pharmacologic Testing: pharmacologic agents (e.g., cocaine, apraclonidine ) to confirm the diagnosis by demonstrating the absence of normal pupillary dilation. • Imaging: MRI or CT scans to identify the underlying cause of the syndrome.

25.  Management and Treatment Managing the underlying condition causing Horner’s Syndrome. • Symptomatic Treatment: artificial tears for dry eyes due to decreased blinking and eyelid surgery for severe ptosis. • Interdisciplinary Approach: importance of collaboration among specialists, including neurologists, ophthalmologists, and potentially oncologists or surgeons, depending on the cause.

26. Thank you