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വാതായനം neurologic clinic ll 09 Oct 2026 — Transcript

by Ayurveda Medical Association of India [Official] · 8,087 words · 1,555 segments · language en · Watch on YouTube

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0:06Neurologic CM series
0:17functional
0:20function
0:26factor
0:29Um amap
0:32district president
0:35doctor secretary of doctor state
0:38committee member
0:42state committee member
0:50neurology It is
1:05Facebook.
1:17for
1:29cosmetology
1:33postpartum treatment
1:37disorders.
1:38Okay.
1:48Neurology.
1:49Correct.
2:00for clinic.
2:21foreign
2:43neurology. Fore
2:54sessions.
3:38district.
3:49Okay.
4:06Dr.
4:10Secretary
4:24Dr. Felt
4:37participation
4:45neurology
4:49session for
5:04topology
5:17workshop.
5:19for
5:47C for
6:00college.
6:10Okay.
6:15schedule.
6:30Participant
6:50participants
6:56series.
7:06Patience patience.
7:08for
7:37speciality.
7:42special
7:55knowledge
7:59orientation. Okay.
8:17Thank you so much.
8:23>> Thank you doctor.
8:30So the medium of class will be in
8:33English. Inauguration session will be in
8:35malam but the medium will be in English.
8:38Uh so
8:43state committee member
8:58session
9:03Dr. Felin
9:35neurological disorders. person
10:05neurology. ological disorders.
10:19Ser
10:35forchech.
11:14for
11:26tips
11:31conventional
11:38nonconventionality.
11:58Dr.
12:00Neurology
12:17particip
12:18free of cost
12:38me
12:45secretary ala
12:52neurology.
13:23for
13:52stroke.
14:06Doctors
14:18windch
14:33uh thank you doctor
14:39district secretary Dr.
14:48for
14:52[sighs]
14:59medical association of India
15:03neurolog.
15:12Okay. [clears throat]
15:52Fore! Foreign! Foreign!
16:13for
16:31Thank you.
16:34Um, thank you Dr. Feler. um
16:49thank you doctor.
16:51Good evening doctors.
16:54Uh it's give me an immense pleasure to
16:56welcome you all to today's section of
16:59the neurologic CMA series. a structured
17:02clinical learning program focusing on
17:04clinical neuro neurology and I
17:07integration. Today uh we will discussing
17:10a clinically relevant and interesting
17:12topic tremors and abnormal movements
17:16from clinical recognition to ayurvedic
17:18approach. Recognizing abnormal
17:21movements, understanding their clinical
17:24significance and developing an
17:26appropriate approach to patient
17:28assessment are important aspects of
17:31clinical practice. It's now uh my
17:34privilege to introduce our esteemed
17:36resource person for today. Dr. Susida SG
17:41Dr. Susida holds a BMS degree and an MD
17:44in Kai Chigsa. She is currently serving
17:47as an assistant professor in the
17:50department of kaigilsa at government
17:52Ayurveda college.
17:55She has valuable experience in clinical
17:57medicine teaching academic consultancy
18:00and research
18:02with the clinical exposure to various
18:04specialties including neurology,
18:07cardiology, hepatology, psych
18:09psychiatry, rheumatology and diabet. She
18:12has also been associated with research
18:15activities at institutions such as
18:18National Ayurveda Research Institute
18:20Cheri. Herademis academic accomplish
18:24include sec securing the university
18:27topper position in MD Ka.
18:30She has also received various
18:32scholarships and awards and has
18:35contributed to academic research to
18:37publications
18:39with her expertise in Kaiigalsa clinical
18:42experience and academic background. We
18:45look forward to an insightful section
18:47exploring the clinical recognition of
18:49tumors and abnormal moments and their
18:52approach within an ayurvedic clinical
18:55framework. On behalf of the organizing
18:57team, I extend a warm welcome to Dr.
19:00Susida and thank her for joining us as
19:03our resource person. Ma'am, we are
19:06delighted to have you with us. I now
19:10invite you to take over the section and
19:12share your valuable knowledge and
19:15clinical insights with us. Thank you.
19:21>> Thank you doctor. Am I audible?
19:24>> Yes, doctor.
19:35Okay.
19:53Tremor and abnormal movement.
19:56Pathophysiology and symptomatology
20:00discussive
20:07session
20:09treaty
20:20discuss
20:24screen share. video.
20:44Screen share.
20:56Hello Dr.
21:01co-host
21:16is it clear to everyone
21:20I am sharing the screen. Uh are you in
21:23disable?
21:26>> Yes. Okay. And let uh moving on to the
21:30section that is tremor and abnormal
21:32movement and integrative ayurvedic
21:35correlation for the practitioners.
21:38The reference text are charida, susta
21:41samida, ashtanga and kadamikraha.
21:47Uh the contents in this class are mainly
21:51the definition and classification
21:56and [clears throat] pathophysiology of
21:58tremor. The evaluation of the
22:20Doctor leech.
22:53Dr.
22:55in the chat box. Uh can we make please
22:58make the screen full screen?
23:18Okay.
23:23>> Is it okay?
23:26>> Yes doctor.
23:28>> Okay. Uh my presentation outlines are
23:31modern perspective that is definition
23:33classification pathophysiology of the
23:35trauma. Uh the clinical evaluation of
23:38the signs and symptoms. Differential
23:40diagnosis and examination of tremor and
23:42abnormal movements. Ayurvedic
23:44perspectives like kambada vyadi nitana
23:48rupa rupa and sambari of kambawadada
23:51vyadi sambari and sus involvement
23:56analysis of movement disorders. A versus
24:01the path modern pathology and the
24:04classic correlation from
24:09these are the glimpse of my presentation
24:12of today's class.
24:16Moving on to the introduction. Tremor
24:18and abnormal movements are the common
24:20neurological presentations encountered
24:22across across the all the age groups.
24:25Modern neurology explains these through
24:28circuit based pathophysiology of the
24:30basal ganglia and the cerebella. These
24:32are the three core areas associated with
24:35movement disorders.
24:37Ayurveda addresses these conditions as
24:40vada predominant disorders under the
24:43broad heading of vadi specifically as
24:46kamba. This is
24:49according to Samita and
24:53according to Ashtanga and
24:56Gadikraha
24:58uh separately describes Kamba or
25:01Kambawada as a disease.
25:05So directly we can enter into tremor.
25:08After that we will discuss about
25:10abnormal movement or uh abnormal
25:13movement disorders and its differential
25:15diagnosis. So uh tremor is a rhythmic
25:18involuntary oscilly movement of the body
25:21part produced by alternating or
25:24synchronous contraction of agonist and
25:27andagonist group of muscles.
25:30These commonly affected parts are arms,
25:33head, legs and the jaw. Typically uh
25:37boys are also involved in some type of
25:39tremors.
25:42Once again, primer is a rhythmic
25:44involuntary oscillatory movement of the
25:47body part produced by alternating or
25:50synchronous contraction of agonist and
25:53antagonistic group of muscles. Commonly
25:56affected parts are the hands, arms,
25:59head, legs and jaw.
26:02Next we can discuss about the basic
26:04mechanisms involved in trouble. First
26:06one is basal ganglia dysfunction. The
26:09common example of basal ganglia
26:11dysfunction and tremor are parkinsonian
26:13tremor. Next one is cerebellar
26:16dysfunction. This is associated with the
26:18cerebila type of tremor or intentional
26:21traumas. Then enhanced physiological
26:23oscillation can be seen in some
26:26physiological conditions like anxiety,
26:28fatigue, caffeines etc. Also you can see
26:33central oscillator dysfunction. It is
26:35associated with the essential drug. Next
26:38one is drug or toxin induced or neuronal
26:42stimulation. You can see association
26:44with the drugs like palpate, lithium,
26:47betaonistic
26:48and stimulants. Then metabolic
26:52disturbances like hypothyroidism,
26:55hypoglycemia, hepatic or renal
26:57dysfunction are also involved in the
27:00pathophysiology of tremor. These are
27:02some differential diagnosis and
27:04mechanisms associated with the tremor.
27:09Then uh we can discuss some more details
27:12about the basic mechanisms in the
27:14pathophysiology of drug. Mainly the
27:17predisposing or provoking factors of
27:19tremor are genetic predisposition, aging
27:22or degeneration, neurodeenerative
27:24disorders, metabolic or endocrine
27:26disorders, drugs or toxins, stress and
27:29anxiety. These are classified as the
27:32predisposing factors or provoking
27:34factors of trauma.
27:36Then we can discuss about the
27:38pathophysiological changes that is
27:41happening in the case of tremor. First
27:43one is dysfunction of the basal ganglia
27:45or the cerebella lead to altered
27:48neurotransmission.
27:50You can see a decrease in the level of
27:52dopamine, decrease in the level of GABA
27:55etc. And this will lead to abnormal
27:59oscilly activity in the motor circuit.
28:03These lead to loss of inhibitory control
28:06and that lead to tremor. The affected
28:10neural circuit are first one is basal
28:14ganglia that is talama cortical circuit.
28:17You can see in the case of parkinsonian
28:20tremor that is resting tremor. Uh the
28:23circute invol basal ganglia talamo
28:26cortical circuit.
28:28The second circuit is cerebellum talamo
28:31cortical circuit that is involved in the
28:33case of action tremor or intentional
28:36tremor.
28:38Then brain stem and spinal circuit. The
28:41third circuit is brain stem and the
28:43spinal circuit. Postural or
28:45physiological tremor is associated with
28:48the uh the uh brain stem and the spinal
28:53spinal circuit associated tr.
28:57The resultant are abnormal rhythmic
28:59involuntary or oscilly activity in the
29:02motor circuit that finally lead to
29:04tremor.
29:06Then next we can discuss about the key
29:09structures involved in the uh
29:11pathophysiology of tremor. First one is
29:13basal ganglia. Basal in the basal
29:16ganglia what are the path pathology
29:19happening in the basal ganglia is there
29:21there will be dopamine deficiency that
29:24lead to altered output signals
29:27in the cerebellum in cerebellar disorder
29:30there will be impaired coordination and
29:32inhibitory dysfunction that is happening
29:34in the case of cerebilar disorders
29:36associated with the trauma
29:39in the talamus if the talamus and cortex
29:42are involved there will be abnormal
29:44osillation conditions and increased
29:46excitability.
29:48Uh I want to say that all these three
29:51structures are not not involved in a
29:54typical type of tremor. In different
29:56type of tremor uh different areas of the
29:59brain are involved according to that
30:01different symptomatology will change.
30:04Then there will be different
30:06neurotransmitters are associated with
30:08the tremor. There will be decrease of
30:10dopamine. There will be decrease of GABA
30:13and there will be increase of glutamate
30:16and there will be altered serotonin and
30:18other neurotransmitters. If dopamine are
30:21decreased you can see parson.
30:23If gaba is decreased you can see this
30:26inhibition and you can see uh difference
30:30in coordination and you can see that in
30:34cerebellar tremor. In the case of
30:36increase of glutamate that is exyitotox
30:39toxicity you can see in talamic and
30:42particle type of tremors you can see
30:44increase of glutamate. Then altered
30:47serotonin and other neurotransmitters
30:49are also associated with the tremor.
30:51[clears throat]
30:51All these contribute to abnormal motor
30:54output that lead to osenatory signals
30:57from the basal ganglia cerebellum and
30:59talamus lead to excessive rhythmic
31:01activation of the motor pathways.
31:04This lead to an altered firing of the
31:08motor circuit of the spinal cube spinal
31:11cord that lead to irregular muscle
31:14activation and inhibition. The clinical
31:16manifestation are tremor. It can be
31:20resting tremor. It can be postural
31:22tremor. It can be action tremor or
31:24intention tremor or others.
31:27Tremor are the alternating contraction
31:30and relaxation of agonist and andagonist
31:33group of muscles. You can see that
31:36amplitude is rhythmic uh typically of 4
31:40to 12 heads or variable.
31:44Then these are all about the basic
31:45mechanism and path of physiology of
31:47drummer. I hope you all are understood.
31:53Next we can discuss when the drummer
31:56occur.
31:59Second point is
32:01why it occur. So uh first we can discuss
32:05when the tremor occur.
32:08Classification of tremor based on the
32:10activation. First one is resting tremor.
32:14Resting tremor present when the body is
32:17relaxed or decreased with the voluntary
32:20movement. It can be seen in Parkinson's
32:22disease. Next one is postural drama. uh
32:26these two are the common tremor that
32:28occur while maintaining a position
32:31against gravity. Postal tremor occur uh
32:34while maintaining a position against
32:36gravity. It can be seen in essential
32:38travel or enhanced physiological tr.
32:42Third one is kinetic tremor. It occur
32:45during voluntary movement. It can be
32:47seen in essential tr.
32:49The other one is intentional.
32:52intentional drummer increases as the
32:55limb approaches the target. It can be
32:58seen typically in cerebellar disorder.
33:01Uh the patient may say that or patient
33:04may show a difficulty uh movement and it
33:08difficulty nearing the target in
33:10approaching or nearing a movement
33:12against the on nearing the target. So
33:16patient may experience tremor and the
33:18patient is not able to uh touch the
33:21target. There may be uh overshooting or
33:24pass pointing can be seen in case of
33:27cerebila disorder.
33:29Then task specific tremor it appears
33:32during a particular skilled activity
33:35while the patient is doing some
33:37particular skilled activity like drummer
33:40like writing that uh like uh playing a
33:44musical instrument etc. The patient may
33:46experience tremor. The fi fifth one is
33:50isometric tremor. It occur during the
33:52muscle contraction without the movement
33:54of the joint.
33:56This tremor occur while gripping an
33:59object. Uh [clears throat] usually the
34:01patients say that uh they will
34:03experience difficulty while gripping a
34:05glass or while holding a spoon for
34:09feeding etc.
34:12These are all about classification of
34:14tremor based on the activation.
34:19Clinical memory aid are resting tremor,
34:22postural tremor, movement tremor and
34:24target oriented tremor. Uh uh resting
34:27tremor occur in the case of Parkinsonian
34:29disease. Postural or action tremor is
34:32associated with the essential tremor.
34:34Intentional tremor is associated with
34:36the cerebellar leion.
34:40So if you are familiar with these points
34:43uh you can easily diagnose uh which part
34:45of the brain is affected.
34:48Next we can discuss why it occur why the
34:52tremor occur.
34:55Classification of tremor based on the
34:57ethiology. It can be categorized into
35:00two. First one is primary causes and
35:02second one is secondary causes.
35:05Uh we can discuss about the primary
35:07causes first that is physiological
35:10tremor. fine rapid low amplitude tremor
35:13associated with the anxiety, fatigue,
35:16exercise and excessive caffeine use. The
35:19main causes are some physiological
35:21causes like anxiety, fatigue, exercise
35:23and caffeine use. The second one is
35:26essential drummer. Essential drummer are
35:29bilateral. Bilateral usually symmetrical
35:32uh postural or action drummer usually
35:35seen in essential drummer syndrome.
35:38hands uh and head voice are affected in
35:41essential tremor. Usually you can see in
35:43aged people over the age of over the age
35:46of 70 to 80 plus you can see essential
35:49trouble.
35:52Uh then parkinsonian tremor mainly these
35:55are resting tremor often asymmetric like
35:58you can see other parkinsonian features
36:00in parkinsonian drummer. It usually
36:03occur in resting position and it reduces
36:05on movement or activity.
36:08The fourth one is cerebellar tremor.
36:11Cerebellar type of tremor are
36:13intentional tremor or kinetic tremor
36:15that worsens on nearing the target. That
36:18is a key point. It worsens on nearing
36:20the target. Uh the cerebellar stroke, MS
36:24or multiple sclerosis tumor or
36:27degeneration affecting the cerebellar
36:29area contribute to cerebilar type of
36:31tremor.
36:32Next one is drug induced tremor. Usually
36:35postural or action tremor. Temporal drug
36:38relationship can be seen. Some there may
36:41be some association with the usage of
36:43drugs like beta aagonist, lithium,
36:46valperate, stimulants and
36:48corticosteroids.
36:50I hope you all are clear about the
36:52primary causes of the tremor.
36:55This will get uh get from the detailed
36:58uh clinical history taking
37:02clinical clue. Uh fine tremor can be
37:05seen in physiological tremor. Bilateral
37:08tremor and symmetrical tremor can be
37:10seen in the in the case of essential
37:12tremor. Resting tremor can be seen in
37:14Parkinsonian tremor. Intentional tremor
37:17can be seen in cerebella disease and
37:20drug own particular drug history or drug
37:24exposure can be seen and associated with
37:26the drug induced tremor.
37:29Uh next we can discuss about the
37:31classification of the driver based on
37:34the uh secondary costs.
37:38First one is metabolic or endocrine
37:40disorders. Fine postural tremor with the
37:43systemic features can be seen in
37:45metabolic or endocrine disorders. You
37:47may be familiar about the
37:48hypothyroidism, hypoglycemia,
37:50electrolyte abnormalities etc. You can
37:53see fine postural tremor associated with
37:55these disease conditions. So on um
37:58ruling rule out by rule out the uh
38:02endocrine causes you can get some uh
38:05abnormality with the thyroid function
38:08test some uh glycemic test and aolite
38:12test etc.
38:14Next one is toxic tremor variable
38:17depending upon the toxin or exposure. uh
38:20while taking the personal history
38:22patient may be associated with alcohol
38:24withdrawal and the patient may be having
38:27occupationally associated with some
38:29heavy metals like lead and there may be
38:32association with some toxins patient may
38:34be see some agricultural work etc and
38:38there may be uh association with the
38:40toxins
38:43uh the third one is distonic tremor
38:45these are irregular jerky and position
38:48dependent tremor
38:49It can be seen in association with the
38:51donia that we will discuss in the next
38:54part of this class.
38:56Fourth one is functional tremor that is
38:59variable, inconsistent, distractable and
39:02entrainable that is functional neur seen
39:05in functional neurological disorder.
39:07There are some structural neurological
39:08disorder and some functional
39:10neurological disorder. Function tremor
39:11are associated with some functional
39:13neurological disorders.
39:16Uh then degenerative or structural
39:19conditions, tremor associated with other
39:21neurological deficit like
39:24neurodeenerative disorders, stroke or
39:27structural lesions etc. These are
39:30associated some neurodeenerative
39:32disorders. One of the example of
39:33neurodeenerative disorder are
39:36Alzheimer's disease uh dementia then uh
39:40PD are example of neurodeenerative
39:43disorder.
39:46So uh remember the secondary tremor is
39:49always you have to look for the ethology
39:52like drug metabolic diseases toxins
39:56structural lesions and functional
39:57causes.
40:00A glimpse into the tremor
40:02classification.
40:03Uh you can see that pisgic tremor are
40:06fine rapid and low amplitude usually
40:09bilateral. The common causes are
40:11fatigue, exercise and excessive cuffing
40:13use. Essential tremor is usually
40:15bilateral postural or action tremor may
40:18be involving the head or voice. Head and
40:21voice are not involved in other type of
40:22tremor. So uh if the drum tremor is
40:25associated with the uh head and voice
40:28you can roll out first the first DD is
40:30essential type of drummer. Parkinsonian
40:33drummer usually dominantly seen on
40:35resting the resting the uh limb in a
40:39particular position.
40:41Often it is asymmetric. The basic
40:43difference is it is asymmetric.
40:46Cerebellar tremor can be differentiated
40:48from other type of tremor like it
40:50worsens while nearing the target. You
40:53can see overshooting or pass pointing
40:55while uh nearing the target.
40:59uh then drug induced tremor usually seen
41:02in some associate you can see some
41:04association with the drugs like lithium
41:06valperate etc.
41:09Then metabolic or endocrine tremor or
41:12fine tremor that is commonly seen and
41:14associated with the conditions like
41:16hypothyroidism hypoglycemia electrolyte
41:19abnormalities etc. Then toxic tremor is
41:22associated with the uh alcohol
41:24withdrawal heavy metals and toxins. The
41:28distonic tremor is usually irregular and
41:30jerky and position dependent commonly
41:32associated with the disease conditions
41:34like donia. Then functional tremor it is
41:38variable and inconsistent usually seen
41:40in functional neurological disorders.
41:42Then degenerative or structural tremor
41:45variable pattern associated with the
41:47neurodeenerative disorder stroke
41:49structural leations etc. Likewise you
41:52can classify the tremor and identify the
41:55you can easily identify the iteology and
41:58the structure involved in the uh in that
42:01type of trauma.
42:03Then clinical examination uh this
42:06clinical examination is common to both
42:09uh tremor and abnormal movement. So
42:12first we will discuss uh the clinical
42:17examination
42:18of both uh tremor and abnormal movements
42:24together.
42:25So I won't discuss about uh the clinical
42:29examination of abnormal movements uh
42:32separately because these uh are common
42:35to each. So uh in this part we can
42:39discuss uh both
42:41a detailed neurological examination
42:44should categorize the movement before
42:46assigning the diagnosis. First you have
42:48to observe the patient assess the onset
42:51and duration of the symptom. The
42:53distribution you have to look for the
42:55symmetry whether it is symmetrical or
42:58asymmetrical. You have to look for the
43:00frequency of the drummer and you have to
43:03assess the amplitude whether it is uh uh
43:05symmetrical or asymmetrical. Uh what is
43:08the amplitude? Usually in the type of in
43:12uh tremor the amplitude is between uh 4
43:15to 12 and the frequency is between 4 to
43:1912.
43:21It is low amplitude. Then you have to
43:24look for the speed, rhythm, pattern of
43:26the trauma, triggering factors,
43:29associated features, relationship
43:31between volness [clears throat]
43:33etc. Observe the patient at rest during
43:36conversation and walking and spontaneous
43:39activity.
43:41You have to look the patient at rest
43:43during the conversation uh while the
43:45patient walking and spontaneous activity
43:48because uh some type of tremor are
43:51usually worsen during conversation
43:54especially anxiety. Some type of tremor
43:57is usually predominant during resting
43:59position like in Parkinsonism.
44:02some type of tremor is associated with
44:04the walking and spontaneous activity
44:07especially in the case of donia while
44:09the patient is taking an appropriate
44:12position uh the trillate
44:16likewise you have to observe the patient
44:19first that is dana dasha and the age and
44:23epic symptoms of the patient have to be
44:26examined through our eyes
44:29first one is dasharisha
44:32Then examine during different
44:34activities. Ask the patient to extend
44:36the arms. The second part is detailed
44:39clinical examination.
44:42Ask the patient to extend the arms. And
44:45you have to perform uh uh you have to
44:48assess the type of trouble
44:51whether it is aggravate or decrease
44:54while extending the arm. Uh then ask the
44:57patient to perform finger nose testing.
44:59Finger nose testing is done by the
45:01patient to uh touch the nose with the
45:04finger that is finger to nose testing.
45:07Then no ping uh from the physician's
45:10hand to the patient's nose
45:14type of testing that is nose finger nose
45:17testing. Then uh ask the patient to tap
45:20the finger perform rapid alternating
45:23movement that is also known as thyroidis
45:26rapid alternating movement.
45:31rapid alternating movements that is
45:34diode that is associated with the these
45:38tests are associated with the balance
45:41and coordination seen in cerebellar
45:43disorders. Ask the patient to write
45:46[clears throat] something uh to look for
45:49the handwriting whether it whether it is
45:51uh patient is having microraphia as seen
45:54in Parkinsonism.
45:56Ask the patient to open normally. Uh
45:58look for the gate whether is any
46:00abnormality with the gate. Uh ask the
46:04patient to perform tantem marking. Uh if
46:06the patient is not able to do tandem
46:08working uh it is maybe having
46:11association with the cerebellar
46:12conditions. Ask the patient to do the
46:15task that precipitate the movement.
46:20Assess uh whether the movement changes
46:22with the voluntary activity,
46:24distraction, mental task, posture or
46:26specific actions. Uh in some conditions
46:29like anxiety, the uh movement may
46:32changes with the mental task, posture or
46:34specific actions.
46:36Also, we can see some distractions or
46:40voluntary activity.
46:42So uh this is a these are the basic test
46:45uh that we have to uh test in in a
46:48patient with the tremor.
46:51Then associ then moving on to the
46:53diagnostic part uh that is associated
46:56neurological signs in tremor. Look
46:59beyond the
47:06is if the tremor is associated with the
47:09other symptoms like spasticity, hyper
47:12reflexia and if the babinsky sign is
47:15positive babinsky sign or plant response
47:18you all all are familiar with the
47:19babinsky sign.
47:22It may be associated with the pyramidal
47:24signs and can be seen in cortical spinal
47:27tract involvement. Then cognitive or
47:30psychiatric disturbances. You can see
47:32some in some psychiatric conditions can
47:34see uh cognitive decline. Some
47:37neurodeenerative condition like
47:38Alzheimer or dementia is associated with
47:40the cognitive decline. There may be
47:43behavioral change, psychiatric symptoms,
47:45personality changes etc. So you have to
47:48look for the cognitive or psychiatric
47:50symptoms while assessing a trauma. The
47:54importance associations are some disases
47:56like Huntington's disease, Wilson's
47:58disease, neurodyenervative disorders
48:00etc. So associated neurological signs
48:03will help to localize the lesion and
48:05narrow the differential diagnosis of the
48:07tremor. So you have to look for these
48:09symptoms so that you can easily localize
48:13uh which part of the brain are affected
48:16or which area or with which uh spinal
48:19root is affected which uh uh circuit in
48:24the brain is affected.
48:28Then uh Parkinsonian tremor uh you can
48:31see other signs like bradicinesia
48:34rigidity resting tremor decreased arm
48:36syncing and short shuffling in the case
48:40of parkinsonian tremor. In the case of
48:42parkinsonian tremor brain or basal
48:44ganglia is mainly involved. Then cereal
48:48tremor you can see atexia dysmetria
48:51disordinia distas and disia. I think you
48:56all are all all are not familiar with
48:58these steps. First I will discuss what
49:01is attackia.
49:15Atexia is a neurological sign or symptom
49:18defined as the loss of full control of
49:20body movement muscle coordination and
49:23balance is a broad term uh of the loss
49:28of full body control of movement muscle
49:30coordination and balance.
49:34The next term is
49:37dysmmetria.
49:39Dismmetry is a neurological condition or
49:42disorder where a person cannot
49:44accurately judge the distance, speed or
49:46power during voluntary movement causing
49:49them to either overshoot that is
49:51hyperria or fall short or hypometria of
49:55a target. This is associated with the
49:57dismantria.
49:59Then disiia.
50:02This diodeia means is the impaired
50:05ability to make the fast alternating
50:08movements smoothly in a coordinated
50:10manner.
50:17These are seen in cerebellar disorders.
50:21Uh in the case of Parkinsonian tremor
50:23you can see resting tremor associated
50:25with the bradicinesia and in the case of
50:28cerebellar disorder you can see
50:29intentional tremor associated with the
50:32atasia and dismia. This can be seen in
50:35cerebellar involvement
50:41resting tremor associated with the
50:43brainia is related with the basal
50:45ganglia dysfunction or panitism.
50:48Intentional tremor associated with the
50:49atexian dysmetri cerebular condition. Uh
50:53tremor with the spasticity and positive
50:56babinsky sign is associated with
50:57pyramidal direct involvement. Tremor
51:00associated with the cognitive or
51:01psychiatric changes can be seen in
51:03neurodeenerative conditions. Metabolic
51:05disorders and psychiatric conditions
51:07like anxiety.
51:10So next we can discuss about the
51:12investigations for tremor. first as CBC
51:15to any rule out anemia, infection and
51:17systemic illness and and identify the
51:20contributing systemic causes. Then you
51:22have to look for the blood glucose level
51:25to assess the hypoglycemia or
51:27hypoglycemia
51:29uh or the metabolic causes of tremor.
51:31And then you have to look for serum like
51:34sodium, potassium etc to detect that any
51:37metabolic or electrolyte disturbances
51:39are associated with the tremor. Then
51:41renal function, liver function test have
51:44to be ruled out. And then thyroid
51:46function test need to rule out
51:48hypothyroidism. Then calcium and
51:50magnesian level have to be ruled out
51:52because metabolic or neuromuscular
51:54dysfunction can be seen in calcium or
51:56magnesium deficiency. And then you have
51:58to look for MRA brain to rule out
52:00structural brain abnormalities.
52:05Then specialized investigations in
52:07tremor uh EEG. uh if there is an you
52:11suspect any epileptic myoclonus or
52:13seizure related movement you can perform
52:17EEG then business disease workup uh
52:20young if the patient is young and if the
52:23tremor or movement disorder is
52:25associated with any hepatic or
52:27psychiatric features uh some
52:29[clears throat] hepatic panel uh
52:32dysfunction and some psychiatric
52:34features are involved in Wilson's
52:35disease so you have to look for special
52:38type test like serum cerillopplasmine
52:41serum copper level 24-hour urinary
52:44copper and
52:46uh case flesher ring case flesher ring
52:50is seen around the cornea as popy ring
52:55uh usually tested on slit lamp
52:57examination.
52:59This is a business disease markup. It is
53:02a young patient associated with the
53:04trauma assoc and having some uh disorder
53:08associated with the liver function test
53:11and patient may show some psychiatric
53:13features.
53:15Then autoimmune evaluation have to be
53:17done to if if you suspect any autoimmune
53:20or inflammatory neurological condition
53:22you have to look for ANA profile and it
53:24is DNA level and if possible liquid
53:26antibodies and other targeted test
53:30because in SLE the neurological
53:33manifestation can be associated with the
53:36tremor.
53:37Genetic testing, strong family or early
53:40onset of inherited disorder. If you are
53:43suspecting this type of uh disorder, you
53:46have to look for uh genetic testing. For
53:48example, Huntington's disease uh testing
53:52and a selected movement disorder genetic
53:55panels uh in a sus in a person with the
53:58strong family history.
54:01Then electrphysiological studies have to
54:03be done. uncertain tremor and abnormal
54:06movement phenomenology you have to look
54:08for EMG to characterize whether it is
54:12tremor or myoclonus
54:16then management of tremor general or
54:18post specific management
54:20uh can be done treat the cause uh drug
54:25induced tremor review or modify the drug
54:29lifestyle measures like reduce the
54:32caffeine us fatigue uh and sleep
54:35deprivation, stress management like
54:38relaxation, adequate sleep and
54:40behavioral measure of anxiety amplified
54:42drummer,
54:44Parkinsonian directed therapy for or
54:47leodopa based treatment according to the
54:49clinical phenotype in parkinsonian type
54:51of tremor. If it is cerebella tremor
54:54underly the disorder and give
54:56rehabilitation it is not completely
54:59curable. So we have to give the
55:01rehabilitative therapy. If the if the if
55:04if it is functional you you have to do
55:07education uh physiootherapy and
55:10psychological intervention. Uh broadly a
55:13multi-disiplinary management is needed
55:16for all these type of disorders.
55:20In the case of essential tremor propanol
55:22or primion is the common first line
55:24management refractory essential tremor
55:27topenomide is given. Parkinsonian
55:29trauma, leodopa or other parkinson
55:31directed therapy can be given. In the
55:33case of drug induced tremor, reduce or
55:35withdraw the offering drug when it is
55:37appropriate. Uh in the case of
55:39cerebilar, treat the cause and give
55:42rehabilitation. If it is a Wilson's
55:44disease associated with the trauma, you
55:47you give copper lowering therapy.
55:50Likewise, uh specific advanced
55:52management will be home.
55:55Next part of our class is abnormal
55:58movements.
56:01The involuntary movements uh that is
56:03definition and clinical meaning. Korea
56:06is brief irregular non-riythmic jerky
56:09movement flowing between the body part.
56:12The clinical meaning of uh cora is
56:15danceike or unpredictable movement.
56:17Classically seen in Huntington's disease
56:19and other facial ganglia disorders. you
56:22can see in Huntington's disease. After
56:26uh discussing the signs and symptoms, I
56:28will show some of the video uh of this
56:31movement disorder because these all are
56:33confusing by uh discussing the symptoms
56:37and definition you you should might not
56:41be possible to uh rule out or
56:45differentiate all these type of movement
56:47disorder. So I will show brief videos of
56:51these movement disorders.
56:54Don second one is donia that is
56:57sustained or repetitive contractions
56:59causing twisting postures. Uh by
57:02definition donia is like this then it is
57:06abnormal muscle contraction or abnormal
57:09posture maybe focal segmental or
57:11generalized.
57:14The third one is myoclonus. You can see
57:16sudden brief shock like involuntary
57:19jerk.
57:21These are very rapid jerk. Maybe
57:23positive contraction or negative or
57:26brief loss of contraction can be seen.
57:29It can be positive or negative usually
57:32associated with epileptic disorders.
57:37Then ticks. Ticks are stereotyped
57:40repetitive movements or sounds open
57:42suppressible. Ticks are suppressible by
57:44ourselves. These are repetitive
57:47patterned movement with premonary urge
57:50and temporary suppressibility. Typical
57:53of tick disorders or toet syndrome.
57:57Atosis, slow ripping continuous
58:00movements usually the dist part of the
58:02limbus associated in the case of atosis.
58:05These are slow bomb like movement
58:08reflecting invaded basal ganglia motor
58:11control often associated with the donia.
58:14Then bismas balismas are large amplitude
58:18violent flinging movements usually
58:20proximal part of the limb are affected.
58:22In the case of atosis distal part of the
58:24limb was affected. Uh balismas usually
58:27proximal part of the limb is associated.
58:30These are high amplitude proximal
58:32flinging movements classically
58:34associated with the subthalamic nucleus
58:37dysfunction. So
58:40um
58:44also in the case of Korea
58:47there is rapid irregular dance-like
58:49movement can be seen. The main causes of
58:51the kora are Huntington's disease, sedan
58:55harms kora, Wilson disease, drug induced
58:58antiscychotics or leodopa, autoimmune or
59:01metabolic disorders. These are rapid
59:04irregular unpredictable movements flow
59:06from one body part to another. There
59:08will be facial primising can be seen,
59:11limb movement can be seen and motor
59:13impersistence can be seen.
59:16uh in the case of atosis you can see
59:19slow ripping movement especially of the
59:22distal part of the limb. You can see it
59:24in the cerebal pulsy, basal ganglia
59:27injury, kicress, hypoxic brain injury,
59:31Wilson's disease, other basal ganglia
59:33disorders etc. Uh these are slow and
59:37continuous especially of the fingers and
59:40hands and feet. Difficulty in
59:42maintaining a stable the patient may
59:44experience difficulty in maintaining a
59:46stable posture.
59:48In your OPD you may be familiar with
59:50cerebral pulsy I think and hypoxic brain
59:54brain injury also common. Uh in both
59:57these condition you can you may be
59:59familiar with the athtosis
1:00:01usually distal part of the limb are
1:00:04affected in the case of atosis.
1:00:07In the case of myoclonus that is sudden
1:00:10shock like jerk can be seen. These are
1:00:12seen in epilepsy, metabolic or toxic
1:00:15disorders, encphylopathy, renal or
1:00:17hypatic dysfunction, hypoxic brain
1:00:19injury, medication side effect,
1:00:21neurodeenerative disorders etc. These
1:00:24are sudden pre shock like jerks, focal
1:00:27or multif focal or generalized. It can
1:00:29be seen at rest or with action or
1:00:31stimulus. Ticks are stereotyped movement
1:00:34or sound. In ticks you can see also see
1:00:38some sound.
1:00:39Primary tick disorder, torture syndrome,
1:00:42neurodedevelopmental conditions,
1:00:43secondary tick drugs or uh neurological
1:00:46disorder are the common causes.
1:00:49Recurrent sudden stereotyped movement or
1:00:52vocalization premonetary urge temporary
1:00:56it is temporarily suppressible and
1:00:58increasing with inner tension.
1:01:01Next uh for a while we can see some
1:01:05videos of this uh
1:01:08this particular type of abnormal
1:01:10movement
1:01:11donia twisting postures and the
1:01:14sustained contraction can be seen uh it
1:01:17can be seen and associated with the
1:01:19genetic conditions cerebral parsy
1:01:21Wilson's disease Parkinson's disease
1:01:23dopamine blocking drug uh toxicity and
1:01:28other acquired brain lesions etc these
1:01:30These are sustained intermittent muscle
1:01:33contraction, twisting movement, abnormal
1:01:35postures, repetit repetitive patterns
1:01:39and uh task specific and drummer may
1:01:42coexist in case of pistonia. Then
1:01:45bismness. Balismas are large amplitude
1:01:48flinging movements. Main causes are
1:01:50contraal, subdalamic leion, uh eshkemic
1:01:53or hemorrhagic stroke, non kerat ketoic
1:01:57hyperglycemia and other structural
1:01:59metabolic causes.
1:02:02These are large amplitude violent
1:02:04flinging movements usually proximal part
1:02:07of the limbar affected typically uh
1:02:09unilateral in case of hemalism there may
1:02:12be risk of injury or exhibition.
1:02:15Next we can see some videos.
1:02:38First we can see Korea.
1:02:42This is a person with the Korea.
1:02:46You can see dance like movement.
1:03:15Stop sharing.
1:03:24Okay.
1:03:26This is a person with Korea.
1:03:39You can see dance like movements
1:03:44si purposing movements.
1:04:40Some of the tremors like intentional
1:04:42tremor you can see
1:04:45flapping tremor in asterexis. These are
1:04:48metabolic tremor that is seen in hpatic
1:04:51condition. These are essential drummer
1:04:53seen on outstretched hand. These are
1:04:56wing baiting drummer seen in Wilson's
1:04:58disease. This is cora. You can see the
1:05:02lesion in the cordic nucleus.
1:05:04This is this is hemi balance. The leion
1:05:07are present in the subthalamic nucleus.
1:05:11This is donia leion in if the lesion is
1:05:14in the basal ganglia. This is donia.
1:05:18The athosis is also the lesion in the
1:05:20piston basal ganglia.
1:05:27Once again you can see
1:05:32intentional trouble
1:05:37clapping type of tremor.
1:05:43Essential tremor
1:05:48wing beating tremor in Wilson's disease
1:05:51cora
1:05:56hemalism
1:06:04doniais
1:06:16etc.
1:06:31Okay, I hope you all are familiar with
1:06:34this.
1:06:42Then uh our part our our aim is to
1:06:45understand these tremor and abnormal
1:06:47movement in relation with our IVIC um
1:06:51symptomatology.
1:06:55First we can correlate the abnormal
1:06:59movements with ayurvea.
1:07:02PIA
1:07:08is happening in the case of Korea.
1:07:10Mainly of is involved in the case of
1:07:13Korea. Unpredictable dance-like
1:07:16movement. Basal ganglia dysfunction is
1:07:18happening in the case of Korea. The
1:07:19chalabuna of uh vada is mainly involved
1:07:23in koda. In donia, you can see sustained
1:07:28repetitive contraction causing twisting
1:07:30postures. You can see
1:07:33associated with
1:07:36disturbance.
1:07:37Usually it is associated with
1:07:40you can correlate with it with some
1:07:45then myoclonus. You can see sudden pre
1:07:48in muscle check. It is uh you can see
1:07:52the association with and tadsha in in
1:07:55myoclotus.
1:07:57In the case of pigs you can see uh these
1:08:00are repetitive abnormal path is there
1:08:03maybe association with the manova
1:08:07in this uh pathology in atosis uh
1:08:12usually slow and ripping movement uh
1:08:17continuous movements and usually dist
1:08:20part of the limb is affected. So it is a
1:08:23va dominant slow and continuous cha is
1:08:26seen in aidtosis. In the case of
1:08:29balismas large amplitude violent jerking
1:08:32or flinging movements can be seen. So
1:08:36can be seen in case of balismus.
1:08:42Next uh we can disc uh you may all have
1:08:46an have a doubt that why vada is
1:08:49predominant why the vada is important.
1:08:53So uh we can discuss about the dsha
1:08:55siddha associated with these movement
1:08:57disorders. So uh why vada is important?
1:09:01Uh it we can say that vada is the
1:09:04principal factor that is responsible for
1:09:07the movement impulse transmission and
1:09:09motor activity.
1:09:12uh mainly uh we can attribute this chala
1:09:19with relevance to abnormal movement. The
1:09:22chalaguna vada is responsible for
1:09:24excessive or involuntary movement.
1:09:28Is responsible for the lack of stability
1:09:30and control. The saguna vada is
1:09:33responsible for the ability to penetrate
1:09:35minute channels and affect the
1:09:37neuromuscular functions. Some uh brain
1:09:40circuit related with the uh
1:09:42pathophysiology of tremor and abnormal
1:09:45movement we can attribute to the sukma
1:09:48of vada
1:09:50can be attributed uh to and conceptually
1:09:54with the and degeneration. In the case
1:09:57of neurodeenerative disorders
1:10:00of vada is involved
1:10:02vada it may aggravate the vada and
1:10:04neuromuscular instability will be
1:10:07happening. uh then kaguna vada mainly
1:10:10contribute conceptually to structural or
1:10:13functional instability in the case of uh
1:10:16doniaas uh you can see and and some
1:10:20atosis etc. You can see some function
1:10:23function structural instability
1:10:26uh it can be correlated or attributed to
1:10:28garaguna of vada.
1:10:32Generally the vada praoba will lead to
1:10:34excessive or irregular gadi that lead to
1:10:37neuromuscular instability lead to
1:10:39abnormal sestta ka or abnormal movement.
1:10:42So normal vada is equal to regulated
1:10:46movement and praguid vada is responsible
1:10:48for excessive or irregular or
1:10:50inappropriate movement.
1:10:54[clears throat]
1:10:57Then uh next we can discuss this vada is
1:11:00important. First we discussed about why
1:11:03vada is important. Then which vada is
1:11:06important. There are different type of
1:11:07vada mainly vana, prana and udhana are
1:11:10directly involved in movement disorders.
1:11:13Vana is associated directly with the gi.
1:11:18Vano
1:11:22most important for the mana is most
1:11:24important for the uh limb movement,
1:11:27muscle coordination, circulation of the
1:11:29motor impulses and generalized chest.
1:11:42So vana is important. Then pranavay.
1:11:45Pranavay is important for neurological
1:11:47coordination, sensory motor integration
1:11:50and higher functions. Particularly
1:11:52relevant when head or mental
1:11:54manifestation coexist.
1:11:58Then udanavada. Udana may be considered
1:12:01when speech and upper body movement are
1:12:04involved. Then both abana and sabana
1:12:07having indirect role while correlating
1:12:10with some metabolic disorders
1:12:13etc. While considering these symptoms
1:12:16abana and sana are indirectly involved
1:12:19in movement disorders
1:12:25lead to gi
1:12:27directly related with the gi
1:12:30muscularkeeal movement. Therefore,
1:12:32vanamada vaguna can be used as a
1:12:35principal conceptual basis for tremor
1:12:38and many hyperinetic movement disorders.
1:12:45Then samra
1:12:48mainly the main involved areana
1:12:52and kaba may be associated according to
1:12:55the cause and phenotype. DSA subtype
1:12:57primarily
1:12:59associated with the prana and udhana
1:13:01according to the localization dia mainly
1:13:05maj
1:13:08are mainly involved rasa and maidus may
1:13:10be involved depending upon the ideology
1:13:14disases like Wilson's disease you can
1:13:15say there may be association with the
1:13:18rasa and maidus in the case of dadu
1:13:20involvement majadu mainly involved in
1:13:23neurodeenerative conditions like uh
1:13:26while uh
1:13:29discussing about the concept of uh
1:13:32shared concept Shar
1:13:35mastisha as maja as it is enveloped by
1:13:39the
1:13:41kapala it can be it can mishka can be
1:13:45correlated as maja according to
1:13:48by considering that point maju is
1:13:51involved in neurodeenerative conditions
1:13:55which is important. Snail may be
1:13:58considered in neurological manifestation
1:14:00or neuromuscular manifestation. Upper
1:14:03motor neuron, lower motor neuron etc can
1:14:06be published as according to our uh
1:14:11stro involved mainly maja shows this
1:14:14manova show this and others show this
1:14:17according to the course these are uh
1:14:21different depending upon patient to
1:14:23patient and based on the differential
1:14:27diagnosis the will differ.
1:14:31There may be you can see Sanka in some
1:14:33cases you can see and you can see both
1:14:36these are in depending upon the ideology
1:14:39and mechanism of the disease.
1:14:43Uh as the principal seat of isasha
1:14:46theana can be correlated
1:14:49can be pashaishtana
1:14:51is maja
1:14:54that is relevant with the moto system
1:14:59in every each and every neurological
1:15:01condition the roamara affected
1:15:07vada is having direct association with a
1:15:10maju etc.
1:15:14uh is you can see some
1:15:17metabolic disturbances in selected
1:15:19cases. uh in other cases there may be
1:15:22directly datadia happening there may be
1:15:25association with the arma there may be a
1:15:28etc based on the pathology roaba may be
1:15:33chuggari in chronic neurodeiserative
1:15:35diseases in acute cases and subaccute
1:15:38cases the scenario may ashukari
1:15:47uh mainly the vad goanas like rupashid
1:15:50alpa
1:15:53These
1:15:54will lead to
1:16:02irregular sudden sustained repetitive
1:16:04movements. Mainly the involved areas
1:16:08and involved are
1:16:12lead to oria
1:16:14based on the underlying pathology
1:16:18then lead to abnormal neuromuscular
1:16:21abnormal or neuromuscular function. The
1:16:24clinical phenotype
1:16:30etc. This will lead to abnormal movement
1:16:33or and trouble.
1:16:38We have discussed about the toshanta.
1:16:41Then next we can discuss about the
1:16:43basand why different movement occur
1:16:46particularly uh used for explaining why
1:16:49abnormal movement have different
1:16:51phenomenology.
1:16:53First is tremor or ka jala leuna mainly
1:16:57involved. This will lead to oscilly
1:16:59involuntary movement due to
1:17:04lead to chala
1:17:08that is lead to irregular unpredictable
1:17:11and rapidly changing chest. Myioonus is
1:17:14associated with the chala and pishnagura
1:17:16that is associated with the sudden brief
1:17:19rapid chest. Tips are associated with
1:17:21the jala and that lead to repetitive
1:17:24stereotyped or abnormal gadi. Donia lead
1:17:28to vada plus kaba and mainly involved.
1:17:33Vada produces abnormal gi while
1:17:35sustained contraction or stability may
1:17:37have
1:17:39atosis
1:17:42involved. Slow continuous and movement
1:17:44will be happening. In the case of
1:17:46balismala
1:17:48and can be seen excessive forceful and
1:17:51high amplitude movement. These are some
1:17:54correlations. So that we can uh in these
1:17:58different conditions we can select drugs
1:18:00having uh the opposite quality of these
1:18:03uh predominant conceptual gona will be
1:18:06having some role in management. That is
1:18:09why I explained uh the gaandanda to each
1:18:13each one of the movement disorders.
1:18:18Vada predominance abnormal GI or
1:18:21abnormal movement taria myocllis or
1:18:24irregular or unpredictable movement can
1:18:26be seen if it is vada plus dadia can be
1:18:31seen in chronic degenerative conditions
1:18:34and movement dysfunction. Vada plus pipa
1:18:36is involved in movement abnormality with
1:18:39the
1:18:41uhna [clears throat]
1:18:42kishna and inflammatory metabolic
1:18:45features. If vada and kaba are mainly
1:18:48associated you can see a you can see
1:18:50stiffness, heaviness, restricted or
1:18:52sustained movement. You can seen in case
1:18:55of Parkinsonian disorders
1:18:58also vada plus and
1:19:01mainly chala plusuru anda can be seen
1:19:05based on secondary modification of the
1:19:07vada driven mixed features
1:19:12can be seen complex these are complex
1:19:15and more resistant to treatment can be
1:19:18seen in complex neurological conditions.
1:19:21Based on this concept you can select uh
1:19:24the some you can uh do the some and
1:19:28select the appropriate truck and plan
1:19:30for appropriate management.
1:19:34Then
1:19:36while discussing about the trad
1:19:45explained about the uh practical
1:19:47management with broad framework
1:19:56and described as described it in
1:20:01so directly they have not discuss about
1:20:04discuss kambabada as a disease.
1:20:07Kadanigra has explained Kambawada as a
1:20:10disease.
1:20:14Mainly uh exposure to excessive uh
1:20:19positive dietary or lifestyle factor
1:20:21lead to vada praoba. Abana vana mainly
1:20:25involved lead to data depletion chiefly
1:20:28maja and aidu are involved lead to maja
1:20:31sahui
1:20:33si and are mainly involved lead to kai
1:20:37manifestation of head feet or speech
1:20:43then next we can correlate a with the
1:20:46concept of obstruction
1:20:49why aa is important because aa occur
1:20:51when normal Movement of vadaha is
1:20:54enveloped or obstructed by other viated
1:20:57dsha or dsa. Dada is having a property
1:21:00like talaguna. When it is obstructed by
1:21:03other viated dshas we can say that there
1:21:06is a or there is obstruction. When the
1:21:09obstructed pada cannot move in its
1:21:12natural path. So there will be
1:21:14forcefully resist intensify its own
1:21:16qualities. uh this produces accelerated
1:21:20disordered movement rather than simple
1:21:22depletion type of father disorder. So
1:21:25Aina explains why come back and
1:21:27persistent persist to get the severity
1:21:29disproportionate to simple datadia. So
1:21:33you have to look for a with other dshas
1:21:36by other dshas tadus malas etc.
1:21:43uh different type of aa in association
1:21:45with the gamba. You can see mainly uh
1:21:48kaba vada can be seen that is heaviness
1:21:51and sitiffness associated with the
1:21:53drummer and slow onset uh can be seen in
1:21:57kapraada.
1:21:58In the case of pitha the patient will be
1:22:01having some neurological signs like
1:22:02burning sensation local type of mom
1:22:05irritability associated with the drummer
1:22:07can be seen in some conditions like
1:22:10hypothyroidism etc and some uh metabolic
1:22:13disorders like Wilson's disease in the
1:22:16case of momsawada localized muscle
1:22:18tremor associated with the stiffness
1:22:22can be seen in some neuro neuromuscular
1:22:25conditions and pyramidal drug
1:22:28involvement. extra in the case of
1:22:30rectava tremor can be associated with
1:22:32the local vascular congestion or
1:22:34discoloration. You can see some
1:22:36connective disorders connective tissue
1:22:38disorders like esties are estated with
1:22:41the drama.
1:22:43So uh in such conditions it can be
1:22:46correlated with the recta.
1:22:51Then sum up the uh treatment principles.
1:22:54I am not entering in depth into the
1:22:56treatment because uh my role in this
1:23:00class is to make you familiar about the
1:23:03symptomatology about the uh sati about
1:23:07the uh close monitoring symptoms about
1:23:11the dsha
1:23:13why which of
1:23:16mainly ignored in particular type of
1:23:18disease in this contest.
1:23:21So uh I will uh briefly explain some of
1:23:25the srai vidana technique or breaking
1:23:28the pathogenesis in this class through
1:23:30this class.
1:23:34Avoidance of the positive dietary and
1:23:36lifestyle factors
1:23:39like
1:23:41measures when obstruction is dominant
1:23:44like appropriate
1:23:47can be done and then nourishing therapy
1:23:51to counter the
1:23:54then to prevent the relapse. These are
1:23:58the some of the samrai vigana techniques
1:24:01to break down the pathogens.
1:24:04Then overview of management approaches
1:24:09followed by shina can [clears throat] be
1:24:12uh broadly uh attributed to vadi
1:24:17shamina basically
1:24:19or vada shamina formulation as per the
1:24:21dsha involvement can be selected.
1:24:26If you suspect any aa you can go for
1:24:28udana. After that uh after uh reducing
1:24:32the aena or after uh getting the
1:24:36symptoms of a clear you can go for a sa
1:24:40yanasti opa
1:24:43etc.
1:24:47Guru aara avoidance of other aggravating
1:24:50factors diseases.
1:24:54The integration of the treatment
1:24:56combining both modern diagnostic clarity
1:24:59with the classical treatment protocol
1:25:01for indiv individualized care. Usually
1:25:05in the management of uh these movement
1:25:07disorders, you have to look for an
1:25:09integrated approach so that both
1:25:12Ayurveda and modern modern medicine can
1:25:15contribute uh both or more more
1:25:19contribute to the management of movement
1:25:21disorders.
1:25:28So uh by this I am concluding my
1:25:32session. Uh tremor and abnormal movement
1:25:35require uh correlating modern
1:25:37pathophysiology with the ayurvedic
1:25:39gaadosha sitada.
1:25:41Uh classify the tadu and show this
1:25:44pathology.
1:25:46uh gamba is uh mainly uh correlated with
1:25:50movement disorders as it is frequently
1:25:54complicated by a uh you have to look for
1:25:57the samra analyze the uh guides precise
1:26:02and individualized samrai vigana can be
1:26:04done in each cases
1:26:06uh mainly modern diagnostic procedures
1:26:11will uh will be required for the
1:26:13accuracy and treatment outcome for the
1:26:16practitioner
1:26:17So that uh I I have given an emphasis to
1:26:22differential diagnosis and investigation
1:26:24procedures.
1:26:26Uh through that we can uh say that uh we
1:26:30can directly uh tell the patient about
1:26:34the prognosis of the disease condition
1:26:36whether it is curable whether it is
1:26:39palable etc.
1:26:41So I hope all you are uh getting
1:26:44familiar about uh tremors and abnormal
1:26:47movements. Thank you.
1:26:53Can we enter into the discussion part?
1:27:09>> Okay. Any doubts you can.
1:27:25Any doubts you can discuss now.
1:28:06Ma'am, good evening. Good evening.
1:28:44Okay.
1:28:47If the patient is associated with some
1:28:49type of movement disorder, patient is
1:28:51not able to perform in a coordinated
1:28:53manner.
1:28:55Either in case of cerebellar conditions
1:28:58either you can see the pass pointing
1:29:00there may be uh associated with the uh
1:29:05coordination difference. They cannot
1:29:08perform in a coordinated manner.
1:29:18This type of
1:29:20caninffect
1:29:40is
1:29:40main area associated with the balance
1:29:42and coordination. So
1:29:48>> okay,
1:29:49thank you ma'am.
1:29:51Okay,
1:29:59this aquar from
1:30:14Adishana is Pakasha. So there will be an
1:30:16involvement of papano also. So there
1:30:18must be direct involvement of a in some
1:30:22condition there may be association with
1:30:23the direct association with a
1:30:27in all the involuntary movements we
1:30:30cannot say that the initial stana is
1:30:33initial stana is pasha generally while
1:30:37discussing the samra we can say that the
1:30:40initial stana is or vector the stana is
1:30:44pquasha
1:30:46in some in Some diseases or some
1:30:49condition trauma is the direct
1:30:50pathology. In such conditions we can say
1:30:53that directly masa maja is involved. In
1:30:56such condition we cannot say that theana
1:30:59is
1:31:00in some metabolic disorders there may be
1:31:02direct involvement with the abanavay
1:31:08s and abanovay may directly involved
1:31:10with the metabolic disorders associated
1:31:13with the movement disorders.
1:31:16I hope you are clear.
1:31:30for
1:31:32differentology.
1:32:06England out
1:32:11chat.
1:32:33Generally,
1:32:42sorry.
1:33:09Foreign
1:33:19speech. Foreign speech. Foreign speech.
1:33:29Any
1:33:41more doubt?
1:34:33chat box.
1:34:39How will be uh the presentations?
1:34:43Presentations.
1:34:45Uh how will be the presentation?
1:34:47Magnesium deficiency in some metabolic
1:34:49disorders uh magnesium and calcium.
1:34:53These are normally associated with the
1:34:56neuronal transmission
1:35:02neuromuscular transmission
1:35:07that is magnesium and calcium.
1:35:10Magnesium
1:35:12indirectly involved Perfect.
1:35:35Magnian deficiency hypomagnesia
1:35:38cause wor muscle trouble. it uh it shows
1:35:41as twitches or cramps uh because mineral
1:35:45help to regulate the nerve impulses and
1:35:47calm the muscle activity.
1:35:50Magnesium
1:35:53regulation that is it act as natural
1:35:56stabilizing agent for the nervous system
1:35:59preventing the excessive calcium from
1:36:01the hyper stimulating nerve cells.
1:36:14symptoms.
1:36:17Low magnesium levelcular
1:36:20hyperexitability
1:36:22that is resulting in postural or resting
1:36:24tremor or muscle spasm and weakness.
1:36:35Usually
1:36:42heavy alcoholic stress
1:36:47inhibitors
1:36:49inhibitor
1:36:52acid reflex dism
1:36:56difference.
1:37:20Okay.
1:37:38Thank you so much doctor.
1:37:41>> Thank you.
1:37:42>> Next we will have a word of thanks. I
1:37:45invade Dr. Sananka for delivering the
1:37:48word of thanks for the session.
1:37:56>> Uh first of all thank you Dr.
1:38:00session
1:38:03different type of tremors.
1:38:13Thanks a lot,
1:38:23Dr. J, Dr. Fisel, Dr. Rajes, Dr.
1:38:42participants.
1:38:45Thank you.
1:38:49Thank you Okay.
1:39:17>> Thank you so much. Good night. the PM.
1:39:27>> Okay, doctor.
1:39:31>> Thank you.
1:39:32>> Good night, doctor. Doctor, thank you.
1:39:36>> Thank you all.

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