This document provides information on different types of tremors, including their causes, characteristics, and pathophysiology. It discusses rest tremor seen in Parkinson's disease and other conditions. It also covers postural tremor, physiological tremor, essential tremor, kinetic tremor, and cerebellar intention tremor. For each type of tremor, the summary highlights key details like involved areas of the brain, typical frequencies, symptoms, and potential treatments.
This ppt describes various movement disorders found commonly in elderly persons. It also describes hyper and hypokinetic disorder categorization with cause and pathophysiology of movement disorders.
This ppt describes various movement disorders found commonly in elderly persons. It also describes hyper and hypokinetic disorder categorization with cause and pathophysiology of movement disorders.
Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.
Dystonia is a movement disorder in which a person's muscles contract uncontrollably. The contraction causes the affected body part to twist involuntarily, resulting in repetitive movements or abnormal postures. Dystonia can affect one muscle, a muscle group, or the entire body.
Amyotrophic lateral sclerosis (ALS), AKA "Lou Gehrig's Disease," is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Motor neurons reach from the brain to the spinal cord and from the spinal cord to the muscles throughout the body. The progressive degeneration of the motor neurons in ALS eventually leads to their death. When the motor neurons die, the ability of the brain to initiate and control muscle movement is lost. With voluntary muscle action progressively affected, patients in the later stages of the disease may become totally paralyzed.
Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.
Dystonia is a movement disorder in which a person's muscles contract uncontrollably. The contraction causes the affected body part to twist involuntarily, resulting in repetitive movements or abnormal postures. Dystonia can affect one muscle, a muscle group, or the entire body.
Amyotrophic lateral sclerosis (ALS), AKA "Lou Gehrig's Disease," is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Motor neurons reach from the brain to the spinal cord and from the spinal cord to the muscles throughout the body. The progressive degeneration of the motor neurons in ALS eventually leads to their death. When the motor neurons die, the ability of the brain to initiate and control muscle movement is lost. With voluntary muscle action progressively affected, patients in the later stages of the disease may become totally paralyzed.
This presentation from Wendy Hendrie looks at how health professionals can help people with MS cope with ataxia. It was presented at the MS Trust Annual Conference in November 2013.
Epilepsy is a common neurological disorders in which there will be an abnormal electrical activities in the brain causing a brief disruption in the communication system of the brain cells.
Epilepsy has a very common symptoms of seizures. A seizure is a sudden rise in electrical activity of the brain. It can involve a part of the brain or the entire brain.
To know more details --> https://www.icliniq.com/articles/neurological-health/what-exactly-is-epilepsy
Chronic progressive external ophthalmoplegiaPS Deb
Chronic progressive external ophthalmoplegia (CPEO) is a descriptive term for a heterogeneous group of disorders characterized by chronic, progressive, bilateral, and usually symmetric ocular motility deficit and ptosis, without pain, proptosis and pupil involvement. Commonly a syndrome of Mitochondrial Cytopathy.
This is a short presentation at Down Town Hospital clinical meeting for DNB Medicine students. It dose not cover the all aspects of stroke care especially Thrombolysis, since it is difficult to practice for Medical specialist, and ischemic stroke is not common in North East India
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Management of Tremor
1. TREMOR
Compiled by
Dr PS Deb MD, DM (Neurology)
Director Neurology GNRC Hospitals
Guwahati, Assam, India
2. TREMOR
Rhythmical, involuntary oscillatory movement of a
body part, produced by either synchronous or
alternating contractions of antagonist muscles (1-
3).
Type:
Rest
Action
Postural
Kinetic
3. TREMOR EVALUATION
History
Age of onset, progression
Family history
Systemic symptoms : diaphoresis, palpitations,
and bowel irregularities
Association: other neurological disease, Drug use
Examination
Rate : Frequency
Amplitude
Location: Part of the body affected
Modification:
Rest (repose)
Actional
Postural (static)
Movement
Task specific
Other factors: Anxiety, exertion, sleep, drugs
Special tests:
Handwriting
Drawing Archimedes spirals
Ability to transfer water between 2 cups or drink
from a cup
Investigation
EMG: Antagonist muscle shows, burst
synchronous / asynchronous
Recording: Acceterometer, Goniometer, Computer
4. PATHOPHYSIOLOGY
Due to burst of α motor neuron, synchrony in antagonistic
muscle, presumably inadequately in the strength and timing of
contraction of opposite muscle group.
Rhythmic burst of discharge of unitary cellular activity in VIM of
thalamus synchronous with tremor on contralateral side with
stopping of tremor by voluntary or passive movement due to
disappearance of burst
The neurons are arranged somatotopically and respond to
kinesthetic impulse from the muscle and joint involved
In monkey VIM contains large sized neuron receive dense
projection from the cerebellar nuclei and spinocerebellar tract
Tremor can be abolished by lesion of VIM
VIM is key nucleus which is sensory in character as well as
interfering motor activity
5. PATHOPHYSIOLOGY
Synchronous burst also occur in sensory-motor cortex,
important for tremor generations.
Passive stretching of muscle →
>1Hz Non Parkinsonian
< 1Hz Parkinsonian
Suggest tremor rhythm is strongly influenced by spinal reflex
mechanism
Pathway not clear pyramidal / extrapyramidal
Probably tremor is produced in the reticular formation
the brain stem or thalamus and is modified and
regulated in its rhythm setting by spinal reflex
mechanism most prominently by the kinesthetic sence.
6. PATHOPHYSIOLOGY
Frequency Site System involved Human form
8-12Hz None Olivocerebellum Physiological
6-8 Hz Dentate N. Olivocerebellum Essential
3-6 Hz Midbrain
tegmentum
Thalamo-cortical Parkinsonism
Lamore 1984 in monkey Hornalive (GABA antagonist) injection
7. Oscillation in
Inf- Olive
Activation of
Purkenji Cells
Reticulospinal,
vestibulospinal,
cerebellothalamic
system
Tremor
Tremor abolished by inf. Olive lesion
But, no such lesion found in human except palatal myoclonus
11. PARKINSONIAN TREMOR
Incidence: 60-70% at the onset(8).
Rate : 3-7Hz variable
Amplitude: moderate
Location: One of both hand→ feet → jaw → tongue
Type:
Flexion extension of hand , adduction abduction of
finger, pronation supination of forearm
Flexion extension of finger + adduction abduction
of thumb – pin rolling tremor
Foot flexion extension
Lips and jaw opening and clossing
Tongue in and out
Eyes flutter when closed
Other type: 15-30%
Fast frequency postural or action tremor
Paralysis agitance: gentle distal tremor
Post encephalatic: proximal slow tremor
Elderly my have tremor for long time without other
features of parkinsonism which may develop later
Progression:
Modification:
Increased
At the time of repose
Emotional stress
Walking
Reduced
when hand is supported
by willed movement
During deep sleep, relaxation
Rigidity
Functional interference
Does not interfere with voluntary movement
Association: other neurological disease
EMG: Antagonist muscle shows, burst synchronous
/ asynchronous
Recording: Acceterometer, Goniometer, Computer
12. PAHTOPHYSIOLOGY
Not due to nigrostriatal dopaminergic deficit
Animal lesion of SN, striatopallidal → no tremor
All patients with SN lesion do not have tremor
Central oscillator in thalamus, cerebellum, globus pallidus, or
subthalamic nucleus,
Monkey: lesion between SN and RN in midbrain tegmentum
→ parkinsonian like tremor (Ward)
Severity may correlates with loss of subgroup of
mesencephalic neurons
A midbrain lesion near the red nucleus can involve the
nigrostriatal pathway in addition to cerebellar outflow tracts
and cause a tremor at rest as well as an action tremor, known
as a Holmes, or rubral, tremor. (5)
13. RX PD TREMOR
Dopamineric agent : 50% reduction with levodopa ,
Amantadine, clozapine, propranolol,and mirtazapine,
Botulinum toxin has been found to effective for some
patients with PD hand tremor (19,20) and jaw tremor
(21).
The subthalamic nucleus is the most common surgical
target for medically refractory PD-related tremor (8)
but lesioning or deep brain stimulation of the thalamic
nucleus ventralis intermedius can also be performed.
A lack of major benefit has been observed with gamma
knife thalamotomy (22).
14. OTHER REST TREMORS
Cerebellar rest tremor: also due to striatonigral lesion
Hereditary chin tremor
Paroxysmal tremor
Dystonic disorder with tremor – spasmodic torticollis – 1-6.5 Hz
Shuttering attack of children
Whole body tremor + sympathetic changes
± Essential tremor or FH of ET
Jittering of new born infent
With other signs of CNS hyperactivity
Hypermobility
Hypertonicity
Easy to startle
Due to pre or post natal insult
16. PHYSIOLOGICAL TREMOR
Asymptomatic oscillation of body
Present even during sleep
Cannot be seen by eyes
Frequency 8-13 Hz
Due to (Marsden)
Mechanical resonance frequency of related joints
Irregularity of muscle contraction in an un-fused tetanus of
slow firing motor unit
Reflexion of balistocardiogram
Oscillation in the spinal monosynaptic reflex
17. ENHANCED PHYSIOLOGIC TREMOR
Frequency :8-13Hz (altered by mechanical
loading, alpha/beta stimulation)
Due to increased operation of segmental stretch
reflex consequent to mechanical changes produced
in the muscles by its beta adgrenergic stimulation
19. OTHER CAUSES OF POSTURAL TREMOR
Dystonia,
Parkinsonism,
Myoclonus,
Kennedy syndrome,
Roussy-Levy syndrome.
Parkinson syndromes may have a postural component,
known as a re-emergent tremor,
Midbrain lesion or cerebellar dysfunction (titubation)
(5).
Psychogenic.
20. ESSENTIAL TREMOR
Inherited, constitutional malady characterized by kinetic tremor in
the absence of other neurological signs
Prevalence – 0.9% increases with age >95years >20%
Onset: childhood or late life
Progression : Unilateral to bilateral and from arm to head after
several year, voice, tongue, leg and trunk can be involved rarely,
slowly progressive with increased severity
It can be hereditary (30%) with variable penetrance or sporadic
and has a bimodal age at onset.
Etiology : Unknown (Genetic, toxic)
Pattern: Kinetic tremor, postural and during action (writing,
drinking,), >50% have intention component, rarely rest tremor
also
21. ESSENTIAL TREMOR
Frequency : 4-12 Hz inversely related to amplitude
Amplitude more than physiological, increases gradually and large
proportion are disabled
Type: Postural action tremor, sometime intentional, rarely rest (frequency
4-12Hz)
Site: Aadduction-abduction movement of the fingers (individual finger can
be affected) and flexion-extension movement of the hands-> Head no-no
(F>M)-> voice and jaw, lower limbs are rarely affected.
Modification: Forment’s sign: Tremor and cog-wheeling increased
voluntary activity even in opposite limbs and reduced by relaxation
Increased by cold, exercise, emotion, sympathetic stimulation
Associated cerebellar features (mild ataxia of gait ), Mild cognitive
difference
23. ASSOCIATED NEUROLOGIC DISEASE
Parkinson’s disease
Higher incidence of PD in
ET 24times
In familial PD ET common
Spasmodic torticollis
Torsion dystonia
Essential myoclonus
Peripheral neuropathy
Fredrick's ataxia
Physiological tremor
Other condition
Essential hypertension
CVD
CHD
Alcoholism
Intelligent professional
24. ESSENTIAL TREMOR TYPE (MARSDEN)
Type I – Benign exaggerated essential tremor (8-12Hz)
Type II – Benign pathological essential tremor (5-7Hz)
Type III – Severe pathological essential tremor (4-6Hz)
frequently spasmodic, not responsive to therapy
Type IV – Symptomatic essential tremor, associated with other
neurological conditions
25. ESSENTIAL TREMOR - RX
Standard Rx: Propranolol, Primidone
Other Rx: Other beta blockers, Topiramate
, Gabapentin , benzodiazepine
Deep brain stimulation: in resistance cases
Ventralis intermedius (Vim)
Thalamotomy not recommended
26. KINETIC TREMOR
Kinetic tremor refers to oscillation
during a visually-guided voluntary
movement (5).
Cerebellar outflow tract disorder
Stroke
Demyelination
Infection or post-infection
Viral, bacterial, fungal, parasitic, prion
Trauma
Neoplastic or paraneoplastic
Endocrinopathies
Hereditary disease
Spinocerebellar ataxias,
Wilson's disease
Medications
Phenytoin, valproate, amiodarone, lithi
um
Heavy metals & toxins
Organic mercury, alcohol, toluene
Midbrain (rubral) tremor
Severe essential tremor
Psychogenic tremor
27. CEREBELLAR TREMOR MILD
Mild (simple) rapid 10Hz distal (unresponsive to INH)
Severe (Rubral – Gorden Holmes 1904) – not rubral but upper
brain stem lesion involving dentato-thalaminc and dentato-olivary
system
Proximal can be distal Arm > Leg, head and trunk can be
involved
Irregular low frequency (3-5Hz)
High amplitude, increased amplitude with prolonged posture
Intention tremor, increased with goal directed movement of
difficult pathway
Perpendicular to the direction of movement
Associated rest tremor due to involvement of different pathway.
29. PATHOPHYSIOLOGY
Dysfunction of cerebellar-based motor control
mechanical oscillation of joints and their muscles,
stretch reflex oscillations through afferent muscle
spindle pathways to the brain, and centrally-located
oscillatory neuronal groups (5).
Cerebellar tremor tends to occur ipsilateral to a lesion of
the deep cerebellar nuclei or outflow tracts through the
superior cerebellar peduncle (5).
It is likely injury to these outflow tracts through the
midbrain that cause the kinetic component of a Holmes,
or rubral, tremor.
30. TREATMENT OF KINETIC TREMOR
Difficult:
CBZ in small trial
Glutethimide in MS
Bnezodiazepine
Baclofen
Botox no use
Tetrahydrocanabinol
5 Hydroxytryptophan
INH 900-1200mg/d with Pyridoxin
Removal of cause
Behavioral modification: wrist weight while eating
Surgical
Thalamotomy or
Deep brain stimulation of the nucleus ventralis intermedius (Vim)
31. CEREBELLAR INTENTION TREMOR
Rhythmic oscillation on reaching the target perpendicular to
the direction of movement
Once the target is reached tremor will cease after 1 sec
(postural tremor will continue once the target is reached)
Frequency 3-5 Hz
Sometime associated with titubation of head and trunk
Interferes with voluntary act
Drugs ineffective
Stereotaxis improve tremor but not function
Adding wt to the limb
Vigorous friction of the joints
32. PERIPHERAL NEUROPATHY WITH TREMOR
Hereditary motor sensory neuropathy with ET
Chronic relapsing neuropathy after 2-3rd relapse 6-8Hz
tremor improve with neuropathy
Paraprotenemia with neuropathy (IgM benign)
Muscles are not weak, motor conduction reduced,
proprioception normal
Recovery phase of GBS
Rarely Diabetic neuropathy
Uremic neuropathy
Porphyria
33. PATHOGENESIS OF TREMOR IN PN
Enhanced physiologica tremor by weakness and
impairment of stretch reflex (Shid et al)
Loss of large fiber sensory function -> imbalance in
the sensory input to the motor neuron pool
(Shahani and Yong)
Primary CNS disorder
Spinocerbellar pathway involved -> impaired central
function
34. WILSON DISEASE
Postural and intension tremor
3-5Hz severe poximally
Can increase amplitude with time
Wing beating tremor at shoulder when abducted at
90 degree and elbow flexed
35. POST TRAUMATIC
Proximal postural and intentional
Following sever head trauma
Stereotactic VIM lesion
Propranolol
36. ALCOHOLIC TREMOR
Exaggerated physiological
Essential tremor – inherited as different tract
3Hz leg tremor - by standing and closing eyes –
ant cerebellar lesion
37. TASK SPECIFIC TREMOR
1. Primary writing tremor
Related to essential tremor, writer’s cramp, dystonia
Alcohol, Propranolol, Anticholinergic improve in some
2. Vocal tremor
1. Related to ET, family history
1. Respond to alcohol, propranolol
2. Not related to ET, no family
1. Does not respond to beta blocker
39. HYSTERICAL TREMOR
Commonly action tremor
May persist in repose
Irregular frequency
Unilateral
Disappear when attention diverted and restart
tremor shift to other parts of body
40. ASTERIXIS
Arrhythmic lapses of sustained posture
Sudden interruption of muscular contraction allow
gravity or inherent elasticity of muscle to produce a
movement when the patient corrects with overshoot
Metabolic encephalopathy
Anticonvulsant
Anticonvulsant
Unilateral Asterixis
Ant. Cerebral occlusion
Thalamotomy
Mid brain lesion
PathophysiologyThere is a poor correlation between tremor and nigrostriataldopaminergic deficit in PD (8,9). Considerable evidence exists to suggest that a central oscillator is involved in the generation of tremor (5). The central oscillator involved in generation of PD rest tremor may potentially be located in the thalamus, cerebellum, globuspallidus, or subthalamic nucleus (5,10) and the presence or severity of tremor in PD may be related to the loss of particular subgroups of mesencephalic neurons (8,11).A midbrain lesion near the red nucleus can involve the nigrostriatal pathway in addition to cerebellar outflow tracts and cause a tremor at rest as well as an action tremor, known as a Holmes, or rubral, tremor. (5)
TreatmentIn PD, rest tremor can be treated most effectively with dopaminergic medications such as levodopa, dopamine agonists, and MAO-B inhibitors, and anticholinergics (5,12). At least 50% of patients experience a reduction in tremor with levodopa (13). Amantadine (14), clozapine (15,16), propranolol (17) and mirtazapine (18) have also been used with some success (12). Botulinum toxin has been found to effective for some patients with PD hand tremor (19,20) and jaw tremor (21). The subthalamic nucleus is the most common surgical target for medically refractory PD-related tremor (8) but lesioning or deep brain stimulation of the thalamic nucleus ventralis intermedius can also be performed. A lack of major benefit has been observed with gamma knife thalamotomy (22).ReferencesDeuschl G, Bain P, Brin M. Consensus statement of the Movement Disorder Society on tremor. Ad Hoc Scientific Committee. MovDisord. 1998;13(Suppl 3):2-23.Puschmann A and ZK Wszolek. Diagnosis and treatment of common forms of tremor. Semin Neurol. 2011 Feb;31(1):65-77.Elble RJ, Koller WC. The definition and classification of tremor. In: Tremor. Eds. The Johns Hopkins University Press, Baltimore and London, 1990:1-9.Findley LJ, Koller WC. Definitions and behavioural classifications. In Handbook of tremor disorders. Eds: Findley LJ, Koller WC. Marcel Dekker Inc, New York, 1995:371-385.Fahn S, Jankovic J, Hallett M (Eds). Tremors: diagnosis and treatment. In: Principles and Practice of Movement Disorders, 2ndedition. Saunders, New York, 2011;389-414.Alty JE, Kempster PA. A practical guide to the differential diagnosis of tremor. Postgrad Med J. Published online June 20, 2011.Lang AE, Zadikoff C. Parkinsonian Tremor. In: Handbook of Essential Tremor and Other Tremor Disorders. Eds: Lyons KE, Pahwa R. Taylor & Francis Group, Boca Raton, 2005:227-41.Dalvi A, Premkumar A. Tremor: Etiology, phenomenology, and clinical features. Dis Mon. 2011;57:109-126.Vingerhoets FJ, Schulzer M, Calne DB, Snow BJ. Which clinical signs of Parkinson’s disease best reflects the nigrostriatal lesion? J Neural Transm Suppl. 1999;56:1-29.Bergman H, Deuschl G. Pathophysiology of Parkinson’s disease: from clinical neurology to basic neuroscience and back. MovDisord. 2002;17(Suppl 3):S28-40.Paulus W, Jellinger K. The neuropathologic basis of different clinical subgroups of Parkinson’s disease. J neuropathol Exp Neurol. 1991;50:743-55.Marjama-Lyons J, Koller W. Tremor-predominant Parkinson’s disease: approaches to treatment. Drugs Aging. 2000;16(4):273-8.Koller WC. Pharmacologic treatment of parkinsonian tremor. Arch Neurol. 1986;43:126-7.Fahn S, Isgreen W. Long term evaluation of amantadine and levodopa combination in parkinsonism by double-blind crossover analyses. Neurology. 1985;25:603-6.Thomas AA, Friedman JH. Current use of clozapine in Parkinson disease and related disorders. ClinNeuropharmacol. 2010 Jan-Feb;33(1):14-6.Bonuccelli U, Cerevolo R, Salvetti S, D’Avino C, Del Dotto P, Rossi G, Murri L. Clozapine in Parkinson’s disease tremor. Effects of acute and chronic administration. Neurology. 1997;49(6):1587-90.Koller WC, Herbster G. Adjuvant therapy of parkinsonian tremor. Arch Neurol. 1987;44:921-3.Pact V, Giduz T. Mirtazapine treats resting tremor, essential tremor, and levodopa-induced dyskinesias. Neurology. 1999;53(5):1154.Pullman SC, Greene P, Pahn S et al. Approach to the treatment of limb disorders with botulinum toxin A: experience with 187 patients. Arch. Neurol. 53, 617-624 (1996).Sheffield JK, Jankovic J. Botulinum toxin in the treatment of tremors, dystonias, sialorrhea and other symptoms associated with Parkinson’s disease. Expert Rev Neurother. 2007;7(6):637-47.Schneider SA, Edwards MJ, Cordivari C, Macleod WN, Bhatia KP. Botulinum toxin A may be efficacious as treatment for jaw tremor in Parkinson's disease. Mov. Disord. 21(10), 1722-1724 (2006).Lim S, Hodaie M, Fallis M, Poon Y, Mazzella F, Moro E. Gamma knife thalamotomy for disabling tremor: a blinded evaluation. Arch Neurol. 2010;67(5):584-8.
PathophysiologyPhysiologic tremor has a mechanical-reflex component, described as passive mechanical oscillation due to underdampened inertial, viscous, and elastic properties of the limbs and other body parts, as well as a smaller 8-12 Hz component associated with modulation of motor unit activity (15). In enhanced physiologic tremor there is participation of the stretch reflex pathways as the response of this pathway to oscillation increases in times of stress and with certain medications (15).
The most common causes of postural tremor are physiologic tremor, essential tremor (ET), and drug-induced tremor, which is a type of enhanced physiologic tremor that can result from the use of numerous medications including beta-agonists, dopaminergic drugs, stimulants, valproic acid, carbamazepine, verapamil, epinephrine, psychiatric drugs, methylxanthines (coffee, tea), cyclosporine, interferon, and flunarizine.(5-7) Other enhanced physiologic tremor etiologies include stress, endocrine disturbance (eg. hypoglycemia, thyrotoxicosis, pheochromocytoma, adrenocorticosteroids), and toxin use (mercury, lead, alcohol withdrawal).
Postural tremor can also be associated with other neurological conditions such as dystonia, parkinsonism, myoclonus, Kennedy syndrome, and other neuropathic conditions including Roussy-Levy syndrome. (5) Parkinson’s disease as well as other Parkinsonian syndromes may have a postural component, known as a reemergent tremor, and postural tremor may also be due to a midbrain lesion or cerebellar dysfunction (titubation) (5). Postural tremor may also be psychogenic.
Essential TremorEssential tremor (ET) is a chronic progressive neurological disease that features postural and action tremor of the arms. The term was first used by European physicians towards the end of the nineteenth century to describe an inherited, constitutional malady characterized by kinetic tremor in the absence of other neurological signs.1 ET is among the most prevalent movement disorders; a meta-analysis of 28 population-based prevalence studies indicated a prevalence across all ages of 0.9%.2 Prevalence increases markedly with age, and especially with advanced age; in some studies, the prevalence among persons aged >95 years was >20%.2 On an etiological level, both environmental (toxic) 3 and genetic factors4 are currently under investigation, although no susceptibility genes have yet been identified.Clinical Features of Essential TremorET is the most common form of pathological postural tremor (8). It can be hereditary or sporadic and has a bimodal age at onset (5). Postural and action tremor may be mistaken as ET, but is actually Fragile X-associated tremor/ataxia syndrome. Careful examination for cerebellar features and gait disturbance in addtion to corroborating family history are required. The frequency of ET varies widely, from 4-12 Hz, and has an inverse relationship with amplitude. It typically involves an adduction-abduction movement of the fingers and flexion-extension movement of the hands (14), and tends to start unilaterally but affects both sides over time. The tongue, head, or voice can be solely affected but tend to occur with hand tremor, and the legs and trunk are infrequently involved (14). ET often also has a kinetic component and severe ET may occur at rest as well.Kinetic arm tremor (i.e., tremor that occurs during voluntary movement) is a common feature of ET. This tremor is usually slightly asymmetric and may be apparent during a broad range of daily activities (e.g., writing, pouring, and eating). Patients may also have postural tremor (e.g., arms outstretched in front of body), though the amplitude of kinetic tremor exceeds that of postural tremor5 and the converse pattern should raise a diagnostic red flag. In approximately one-half of ET patients, the kinetic tremor may have an intentional component as well (i.e., during finger-nose-finger maneuver, tremor terminally worsens when approaching the target).6 The amplitude of the kinetic tremor increases over time, with recent estimates indicating a median annual increase of ~2.0%.7 Studies have shown that more than 90% of ET patients who come to medical attention report disability 8 and severely-affected end-stage patients are physically unable to feed or dress themselves.9Tremor may additionally involve other body regions. Most common among these is head tremor, which more typically is a side-to-side (”no-no”) tremor, and is particularly prevalent among women with ET.10 Jaw and voice tremors are also common in ET.11 A characteristic feature of ET is the somatotopic spread of tremor over time such that head tremor typically evolves several years after the onset of arm tremor, and the converse pattern raises another diagnostic red flag.9Patients with ET can also develop a tremor at rest without other features of Parkinson’s disease.12 Aside from tremors, a variety of additional (i.e., accessory) motor features have been described in patients with ET and these features all point towards an underlying abnormality of the cerebellum or of the cerebellar system. The most clinically-evident of these features is gait ataxia, which is generally but not always mild.10, 13
The origin of essential tremor is unknown. A centrally-located oscillator has been suggested by electrophysiologic studies and the inferior olive and cerebellum have been implicated by positron electron topography studies (16).
Numerous studies have now demonstrated mild cognitive differences between ET patients and controls, 14 indicating that this is a disease characterized not only by motor but also by non-motor features. The clinical import of these cognitive deficits is not entirely clear, although, studies now indicate that these cognitive features are not without clinical correlates.15 A broad array of neuroimaging studies (functional magnetic resonance imaging, positron emission tomography, [1H] magnetic resonance spectroscopic imaging, diffusion tensor imaging, voxel based morphometry) now indicate the presence not only of functional and metabolic abnormalities in the ET cerebellum, but of structural abnormalities in both the cerebellar gray and white matter.16 In postmortem studies, the degenerative changes in ET are thus far all localized to the cerebellum itself (esp. to Purkinje cells) or to a set of brainstem neurons that synapse directly with Purkinje cells,16 further reinforcing the notion that the disease seems to be one that is centered in the cerebellum and its fiber tracts.Propranolol, which is a nonselective β-adrenergic receptor antagonist, and primidone, an anticonvulsant, remain the two standard treatments for ET. Studies show that a limited number of other agents, including topiramate, gabapentin and several other β-adrenergic receptor antagonists are also beneficial. Surgical interventions, such as thalamic deep brain stimulation, play a role when pharmacological treatment is not satisfactory. References essential tremorLouis ED, Broussolle E, Goetz CG, Krack P, Kaufmann P, Mazzoni P. Historical underpinnings of the term essential tremor in the late 19th century. Neurology 2008;71(11):856-859.Louis ED, Ferreira JJ. How common is the most common adult movement disorder? Update on the worldwide prevalence of essential tremor. Mov Disord;25(5):534-541.Louis ED. Environmental epidemiology of essential tremor. Neuroepidemiology 2008;31(3):139-149.Deng H, Le W, Jankovic J. Genetics of essential tremor. Brain 2007;130(Pt 6):1456-1464.Brennan KC, Jurewicz EC, Ford B, Pullman SL, Louis ED. Is essential tremor predominantly a kinetic or a postural tremor? A clinical and electrophysiological study. MovDisord 2002;17(2):313-316.Deuschl G, Wenzelburger R, Loffler K, Raethjen J, Stolze H. Essential tremor and cerebellar dysfunction clinical and kinematic analysis of intention tremor. Brain 2000;123 ( Pt 8):1568-1580.Louis ED AA, Gillman A, Gerbin M, Viner AS. Estimating annual rate of decline: Prospective, longitudinal data on arm tremor severity in two groups of essential tremor cases. J Neurology Neurosurg Psychiatry 2010 (in Press).Louis ED, Barnes L, Albert SM, et al. Correlates of functional disability in essential tremor. MovDisord 2001;16(5):914-920.Critchley M. Observations of essential (heredofamilial) tremor. Brain 1949;72:113-139.Hubble JP, Busenbark KL, Pahwa R, Lyons K, Koller WC. Clinical expression of essential tremor: effects of gender and age. MovDisord 1997;12(6):969-972.Louis ED, Rios E, Applegate LM, Hernandez NC, Andrews HF. Jaw tremor: prevalence and clinical correlates in three essential tremor case samples. MovDisord 2006;21(11):1872-1878.Rajput AH, Rozdilsky B, Ang L, Rajput A. Significance of parkinsonian manifestations in essential tremor. Can J NeurolSci 1993;20(2):114-117.Stolze H, Petersen G, Raethjen J, Wenzelburger R, Deuschl G. The gait disorder of advanced essential tremor. Brain 2001;124(Pt 11):2278-2286.Benito-Leon J, Louis ED, Bermejo-Pareja F. Population-based case-control study of cognitive function in essential tremor. Neurology 2006;66(1):69-74.Louis ED. Functional correlates of lower cognitive test scores in essential tremor. Mov Disord;25(4):481-485.Louis ED. Essential tremor: evolving clinicopathological concepts in an era of intensive post-mortem enquiry. Lancet Neurol;9(6):613-622.Treatment postural tremorTreatment of postural tremor may involve discontinuing a culprit medication or treating an underlying metabolic condition if an enhanced physiologic tremor is diagnosed. A practice parameter for treatment of ET has been published by the American Academy of Neurology (17). Propranolol (160-320 mg/d, starting dose 20-80 mg/d) and primidone (250-750 mg/d, starting dose 25mg/d) have been shown to have equivalent efficacy for limb tremor and a combination of both may be more effective than each one alone (18,19). Gabapentin, topiramate, alternative beta-blockers, and benzodiazepines may also be helpful (5,20) and botulinum toxin has shown benefit for essential hand tremor (21) as well as vocal (22) and head tremor (23). Alcohol has a beneficial effect for treatment of ET but its use is limited by the short duration of response, potential for tolerance, and risk of alcoholism (20,24). Finally, stereotactic surgery including deep brain stimulation of the thalamic nucleus ventralis intermedius (Vim) and Vim thalalmotomy for medically intractable moderate to severe ET may reduce tremor by up to 90%. There is currently insufficient evidence to recommend gamma knife thalamotomy as a treatment for ET (25).References postural tremorDeuschl G, Bain P, Brin M. Consensus statement of the Movement Disorder Society on tremor. Ad Hoc Scientific Committee. MovDisord. 1998;13(Suppl 3):2-23.Puschmann A and ZK Wszolek. Diagnosis and treatment of common forms of tremor. Semin Neurol. 2011 Feb;31(1):65-77.Elble RJ, Koller WC. The definition and classification of tremor. In: Tremor. Eds. The Johns Hopkins University Press, Baltimore and London, 1990:1-9.Findley LJ, Koller WC. Definitions and behavioural classifications. In Handbook of tremor disorders. Eds: Findley LJ, Koller WC. Marcel Dekker Inc, New York, 1995:371-385.Fahn S, Jankovic J (Eds). Tremors: diagnosis and treatment. In: Principles and Practice of Movement Disorders, 2nd edition. Saunders, New York. 2007;389-414.Alty JE, Kempster PA. A practical guide to the differential diagnosis of tremor. Postgrad Med J. Published online June 20, 2011.Crawford P, Zimmerman EE. Differentiation and diagnosis of tremor. Am Fam Physician. 2011;83(6):697-702.Dalvi A, Premkumar A. Tremor: etiology, phenomenology, and clinical features. Dis Mon. 2011;57:109-26.Lou JS, Jankovic J. Essential tremor: clinical correlates in 350 patients. Neurology. 1991;41:234-8.Elble RJ, Koller WC. Tremor. The Johns Hopkins University Press, Baltimore.Sanes JN, Hallett M. Limb positioning and magnitude of essential tremor and other pathological tremors. MovDisord. 1990;5(4):304-9.Leehey MA. Fragile X-associated tremor/ataxia syndrome: clinical phenotype, diagnosis, and treatment. J Investig Med. 2009;57:830-6.Louis ED, Faust PL, Vonsattel JP, . Neuropathological changes in essential tremor: 33 cases compared with 21 controls. Brain. 2007;130:3297-307.Koller WC and Busenbark KL. Essential tremor. In: Movement Disorders: Neurologic Principles and Practice. Eds: Watts RL, Koller WC. McGraw-Hill. New York:365-85.Elble RJ. The pathophysiology of tremor. In: Neurologic Disorders: Principles and Practice. McGraw-Hill, New York, 2004:481-493.Deuschl G, Elble RJ. The pathophysiology of essential tremor. Neurology. 2000;54(11):S14-20.Zesiewicz TA, Elble R, Louis ED, Hauser RA, Sullivan KL, Dewey Jr RB, Ondo WG, Gronseth GS, Weiner WJ. Practice parameter: therapies for essential tremor: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2005;64:2008-20.Gorman WP, Cooper R, Pocock P, Campbell MJ. A comparison of primidone, propranolol, and placebo in essential tremor, using quantitative analysis. JNNP. 1986;49:64-8.Koller WC, Royse VL. Efficacy of primidone in essential tremor. Neurology. 1986;36:121-4.Dalvi A. Medical treatment of tremor. Dis Mon. 2011;57:135-141.Brin MF, Lyons KE, Doucette J, Adler CH, Caviness JN, Comella CL, Dubinsky RM, Friedman JH, Manyam BV, Matsumoto JY, Pullman SL, Rajput AH, Sethi KD, Tanner C, Koller WC. A randomized, double masked, controlled trial of botulinum toxin type A in essential hand tremor. Neurology. 2001;56:1523-8.Pahwa R, Busenbark K, Swanson HE, et al. Botulinum toxin treatment of essential head tremor. Neurology 1995;45: 822-824.Kendall KA, Leonard RJ. Interarytenoid muscle botox injection for treatment of adductor spasmodic dysphonia with vocal tremor. J Voice. 2011;25(1):114-9.Schroeder D, Nasrallah HA. High alcoholism rate in patients with essential tremor. Am J Psychiatry. 1982;139:1471-3.Deuschl G, Raethjen J, Hellriegel H, Elble R. Treatment of patients with essential tremor. Lancet Neurol. 2011;10:148-61.
Clinical Features of Kinetic TremorKinetic tremor is typically proximal but can be distal (9). It tends to be irregular with high amplitude and low frequency. The frequency of kinetic tremor is commonly reported as 3-5 Hz (10) but it may range between 3-8 Hz in the arms and is usually 3 Hz in the legs (11). It is often called an intention tremor since the tremor usually increases as the tremulous limb approaches a visually-guided target (8). The axis of the tremor depends upon limb position and the movement executed (11), usually perpendicular to the direction of movement (5).
PathophysiologyCerebellar kinetic tremor may be due to dysfunction of cerebellar-based motor control affecting multiple oscillatory mechanisms, which include mechanical oscillation of joints and their muscles, stretch reflex oscillations through afferent muscle spindle pathways to the brain, and centrally-located oscillatory neuronal groups (5). Cerebellar tremor tends to occur ipsilateral to a lesion of the deep cerebellar nuclei or outflow tracts through the superior cerebellar peduncle (5). It is likely injury to these outflow tracts through the midbrain that cause the kinetic component of a Holmes, or rubral, tremor.
TreatmentTreatment of kinetic tremor is often unsuccessful or suboptimal. Removal of the underlying cause by cessation of a culprit substance or management of a tumor or abscess can lead to tremor improvement or resolution. Behavioral modifications may help to dampen kinetic tremor. For example, significant functional improvement has been demonstrated when wrists weights were used by patients with kinetic tremor while eating (12). No drugs have been shown to reduce cerebellar kinetic tremor satisfactorily and reproducibly (6). Small trials have indicated that carbamazepine may reduce tremor amplitude (13) and that levetiracetam may be effective (14). Propranolol use has had varying results (15,16) and treatment with primidone in two patients with multiple sclerosis showed a reduction in cerebellar tremor with improved hand control (17). Evidence for isoniazid has been mixed (5) and its side effect profile may limit its use. An open trial of Glutethimide showed improvement in kinetic tremor due to multiple sclerosis and traumatic brain injury (18). Benzodiazepines and baclofen have both been reported to elicit an improvement in kinetic tremor (19-21) and on open label study of buspirone also showed effectiveness in mild to moderate cerebellar tremor (22). Botulinum toxin type A has been tried for cerebellar kinetic tremor due to multiple sclerosis and no significant improvement was demonstrated (23). Patients with cerebellar tremor who underwent thalamotomy or deep brain stimulation of the nucleus ventralis intermedius (Vim) have experienced improvement (5,24,25).ReferencesDeuschl G, Bain P, Brin M. Consensus statement of the Movement Disorder Society on tremor. Ad Hoc Scientific Committee. MovDisord. 1998;13(Suppl 3):2-23.Puschmann A and ZK Wszolek. Diagnosis and treatment of common forms of tremor. Semin Neurol. 2011 Feb;31(1):65-77.Elble RJ, Koller WC. The definition and classification of tremor. In: Tremor. Eds. The Johns Hopkins University Press, Baltimore and London, 1990:1-9.Findley LJ, Koller WC. Definitions and behavioural classifications. In Handbook of tremor disorders. Eds: Findley LJ, Koller WC. Marcel Dekker Inc, New York, 1995:371-385.Seeberger LC, Hauser RA. Cerebellar Tremor. In: Handbook of Essential Tremor and other Tremor Disorders. Taylor & Francis, Boca Raton, 2005:227-41.Fahn S, Jankovic J, Hallet M (Eds). Tremors: diagnosis and treatment. In: Principles and Practice of Movement Disorders. Saunders, New York, 2011;389-414.Manyam BV. Uncommon forms of tremor. In: Movement disorders: neurological principles and practice 2nd Ed. Eds: Watts RL, Koller WC. McGraw-Hill, New York, 2004:459-80,Alty JE, Kempster PA. A practical guide to the differential diagnosis of tremor. Postgrad Med J. Published online June 20, 2011.Liu x, Miall RC, Aziz TZ, Palace JA, Stein JF. Distal versus proximal arm tremor in multiple sclerosis assessed by visually guided tracking tasks. J NeurolNeurosurg Psychiatry. 1999 Jan;66(1):43-7.Dalvi A, Premkumar A. Tremor: etiology, phenomenology, and clinical features. Dis Mon. 2011;57:109-26.Elble RJ, Koller WC. Cerebellar tremor. In: Tremor. Eds. The Johns Hopkins University Press, Baltimore and London, 1990:109-17.Aisen ML, Arnold A, Baiges I, Maxwell S, Rosen M. The effect of mechanical damping loads on disabling action tremor. Neurology. 1993;43(7):1346-50.Sechi GP, Zuddas M, Piredda M, Agnetti V, Sau G, Piras ML, Tanca S, Rosati G. Treatment of cerebellar tremors with carbamazepine: a controlled trial with long-term follow-up. Neurology. 1989;39:1113-5.Saponara R, Greco S, Proto G, Trubia T, Domina E. Levetiracetam improves intention tremor in fragile x-associated tremor/ataxia syndrome. ClinNeuropharmacol. 2009;32(1):53-4.Braham J, Sadeh M, Turgman J, Sarova-Pinchas I. Beneficial effect of propranolol in familial ataxia. Ann Neurol. 1979;5(2):207.Koller WC. Pharmacologic trials in the treatment of cerebellar tremor. Arch Neurol. 1984;41:280-1.Henkin Y, Herishanu YO. Primidone as a treatment for cerebellar tremor in multiple sclerosis – two case reports. Isr J Med Sci. 1989;25(12):720-1.Aisen ML, Holzer M, Rosen M, Dietz M, McDowell F. Glutethimide treatment of disabling action tremor in patients with multiple sclerosis and traumatic brain injury. Arch Neurol. 1991;48(5):513-5.Trelles L, Trelles JO, Castro C, Altamirano J, Benzaquen M. Successful treatment of two cases of intention tremor with clonazepam. Ann Neurol. 1984;16(5):621.Brunberg JA, Jacquemont S, Hagerman RJ, Berry-Kravis EM, Grigsby J, Leehey MA, Tassone F, Brown WT, Greco CM, Hagerman PJ. Fragile X premuation carriers: characteristic MR imaging findings of adult male patients with progressive cerebellar and cognitive dysfunction. AJNR Am J Neurol. 2002;23(10)1757-66.Weiss N, North RB, Ohara S, Lenz FA. Attenuation of cerebellar tremor with implantation of an intrathecal baclofen pump: the role of gamma-aminobuytricacidergic pathways. Case report. J Neurosurg. 2003;99(4):768-771.Lou JS, Goldfarb L, McShane L, Gatev P, Hallet M. Use of buspirone for treatment of cerebellar ataxia An open-label study. Arch Neurol. 1995;52(10)982-8.Clarke CE. Botulinum toxin type A in cerebellar tremor caused by multiple sclerosis. Eur J Neurol. 1997;4(1):68-71.Shahzadi S, Tasker RR, Lozano A. Thalamotomy for essential and cerebellar tremor. StereotactFunctNeurosurg. 1995;65:11-7.Schulder M, Sernas TJ, Karimi R. Thalamic stimulation in patients with multiple sclerosis: long-term follow-up. StereotactFunctNeurosurg. 2003;80:48-55.