This document discusses gait disorders and their causes. It defines normal gait and describes the gait cycle. It then discusses various types of abnormal gaits such as sensory ataxia caused by disturbances in sensory input, cerebellar ataxia presenting with wide-based staggering gait, and spastic gait caused by lesions interrupting the corticospinal pathway. It also covers parkinsonian gait, multisystem atrophy presenting with features of both parkinsonism and cerebellar ataxia, and spinocerebellar ataxia which is an inherited condition. Various causes of acquired and inherited ataxias are described.
Detailed description of clinical examination of higher mental functions like conscoiusness, cognition, memory, pereception,etc. in neurological conditions.
Detailed description of clinical examination of higher mental functions like conscoiusness, cognition, memory, pereception,etc. in neurological conditions.
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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
- 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
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
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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.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
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- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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2. Gait
• Defined as Bipedal, biphasic , forward
propulsion of centre of gravity of the human
body, in which there are alternate sinuous
movements of different segments of body
with least expenditure of energy.
• In humans two thirds of total body weight is
centered in the upper body which makes for
inherent instabilty.
3. • The limits of stability have
been defined as an inverted
cone with the apex at the
feet and base defining
perimeter at the head .
• Sway outside of this
perimeter results in
instabilty. The dimensions
of the base of the cone are
roughly 12.5 degrees in
anteroposterior diameter
and 16 degrees laterally
4. Requirement for normal gait
Antigravity support of the body
Stepping
Maintenance of equilibrium
Propulsion
5. GAIT CYCLE
• A gait cycle consists of two
steps or one stride ‘the
activities that occur from
the point of initial contact
of one lower extremity to
the point at which the
same extremity contacts
the ground again ‘
• During one gait cycle, each
extremity passes through
two phases, a single
stance phase and a single
swing phase
6. Components of stance phase
• Stance phase comprises 60% of the gait cycle
• Heel strike – moment when the heel first strikes
the ground
• Foot flat – from heel strike to when the full foot is
in contact with the ground
• Midstance – body weight is directly over the
stance leg
• Heel off – moment the heel of the stance leg
leaves the ground
• Toe off – when only the toe of the stance leg is in
contact with the ground
7.
8. Components of the Swing Phase
• Swing phase comprises 40% of the gait cycle
• Acceleration – the toe of the stance leg leaves the
ground and begins to swing forward
• Midswing – the swinging leg is directly beneath
the body
• Deceleration – the swinging leg continues
forward towards knee extension but is slowing
down as it travels, stopping just prior to full knee
extension and heel contact with the ground
14. Gait disturbances can arise from disorders of
• Frontal lobe lesions
• Sensory pathways (sensory ataxia )
• Cerebellum
• Posterior column, dorsal root ganglia, peripheral
nerves
• Extrapyramidal system
• Vestibular system
15. SENSORY ATAXIA
• Disturbances in the sensory input to the
cerebellum
• The nervous system is deprived of sensory
information primarily proprioception and joint
position sense
• Romberg sign
• Loss of tendon reflexes
• Features of peripheral neuropathy
• WIDE BASED HIGH STEPPAGE GAIT
16. • 26 year old female , presented with C/0
progressive tingling/ numbness, weakness,
Ataxia with high steppage gait. On
examination there was spastic parapersis with
extensor plantar. Sensory examination
revealed diminished touch, pressure, vibration
and proprioception.Rombergs test was
positive.
17. • 8 year old male present ed with C/o
Progressive ataxia , with weakness of limbs
and frequent falls, visual impairment with
incoordination.On examination patient had
scoliosis , spasticity , plantar was extensor ,
knee and ankle reflexes were absent with
foot deformity . Sensory examination revealed
decreased proprioception and vibration.
19. • CAUSES OF SENSORY ATAXIA:
Causes-subacute combined degeneration of the
cord (vit B12 deficiency), diabetes sensory
neuropathy
tabes dorsalis, Friedreich ataxia, cervical
spondylosis , meningioma
20.
21.
22. Cerebellar Ataxia
• Wide based gait, clumpsy, staggering, unsteady,
lurching titubating
• The patient is unable to walk in a straight line , tandem
walking is impaired
• With hemispheric lesion the patient will stagger and
deviates towards the involved side
• With lesion of cerebellar vermis,the patient will exhibit
a lurching, staggering gait, but without laterality
• Cerebellar ataxia is present with both eyes open and
closed( romberg negative)
32. • 54 year old male recently diagnosed diabetic and hypertensive came with
complaints of acute onset dhe noticed progressively He gradually developed
progressive truncal ataxia with ataxic dysarthria and intentional tremor, rapidly
worsening over a period of 2 weeks.on examination . Prominent ataxic dysarthria,
dysmetria of upper limbs more than lower limb, dysdiadochokinesia and
intentional tremors were observed. No cranial neuropathy . Upper and lower limb
power was 5/5, with brisk tendon reflexes, hypotonia in the upper limbs and mild
spasticity in the lower limbs.No chronic medication intake.
• On MRI inital3 weeks of illness was normal. All hematological and biochemical
parameters were within normal limits. ANA, Anti DSDNA, APLA, Canca, Panca, CSF
analysis were within normal. CSF electrophoresis was negative for oligoclonal
bands and malignant cells. CSF Cr Ag, PCR-TB, HSV I and II and arbovirus were
negative. A 4cm lympnode was palpable over the axilla. Lymphnode biopsy
revealed hogkins lymphoma . Anti TR anti body was performed was found to be
positive. Mri was repeated showed hyperintensites in bilateral cerebellar
hemisphere.
• Patient was treated with 6 cycles of chemotherapy. Treatment options are limited
and are largely dependent on treating the underlying malignancy to lower
antibody titers. Other therapeutic interventions such as intravenous
immunoglobulins, plasmapheresis and immunosuppressive therapy
34. AUTOIMMUNE CAUSES
• Paraneoplastic Syndromes
- Anti HU abs – small cell cancer lung (
extrapyramidal signs)
- Anti YO Abs – ovarian cancer
- Anti Ri abs – breast cancer
- Anti Tr Antibody – hodgkins lymphoma
35. • 60 year old man presented with
incoordination of movements with tremor ,
with wide based staggering gait , nystagmus
and scanning speech. He gives a history than
his 32 year old son has similar complaints. On
examination power is normal, Tone is
spastic,knee and ankle reflex was absent
plantar was extensor. Dymmetria,
dysdiadakinesis , pendular knee jerk was
present. MRI showed diffuse cerebellar
atrophy
36. Spinocerebellar Ataxia
• Autosomal dominant
• SCA 1-36 types , SCA1,2,3,7,17 due to CAG
triplet repeat expansion codes for glutamine
Protiens termed as ATAXINS- more than -40
glutamines potentially toxic for the neurons –
leads to neuronal loss and gliosis SCA 8- CTG
repeat,SCA 10 forms pentanucleotide repeats
• Anticipation ( earlier age on onset and
aggressive course in successive generation )
37. • SCA 1 middle life progressive cerebellar ataxia
,scanning sppech, nystagmus , dysarthria mild
spascity , parkinsonian tremor , knee and
ankle reflexes are lost. Extensor plantar
response. Urinary and Fecal incontinence.
Variable loss of purkinje cells. Gross atrophy of
cerebellum
• SCA2- onset 2-65 years , ataxia , dysarthria,
parkinsonian rigidity, optic atrophy and retinal
degeneration
• Most common in India
38. • MachadoJoseph disease (SCA3)
• Type 1 (amyotrophic lateral sclerosis-parkinsonism-
dystonic type)
- Weakness , spasticity, broad based lurching gait, ankle and
patellar clonus. Extensor plantar.ophthalmoparesis and
ocular prominence is early manifestion.
- There is no truncal titubation
- Prominence of horizontal and vertical nystagmus
- Loss of fast saccadic movements of eye
- Facial fasciculation,facial myokymia, lingual fasciculation
without atrophy
39. - Type 2 MC ( ataxia type)
- 2 nd and 3 rd decade with corticospinal and
extrapyramidal symptoms
- Dysarthria,cerebellar defects,opthalomoparesis, facial
myokymia, facial fasciculation ,spasticty is present
- Type 3 MJD ( Ataxia- Amyotrophic type )
- Mean age on onset 25 years
- Pancerbellar (dysarthria/ gait distubance)
- Distal sensory loss with features of peripheral neuropathy
(loss of deep tendon reflexes )
- No extrapyramidal or corticospinal involvement
40. • SCA 6:
• Late onset AD ataxia
• Loss of vibration and proprioception
• Familial hemiplegic migraine
• Cerebellar atrophy
• SCA7:
• Presence of retinal pigment degeneration
41. • 55 year old male hypertensive and Diabetic
came with C/O weakness of right upperlimb
and lowerlimb. On examination BP was
240/110 mm hg there was hypertonia ,
spasticity , plantar on right was extensor and
left was flexor. CT head was revealed
hemorrhage involving the internal capsule.
• GAIT ? Circumduction / Spastic gait
42. Spastic gait
• Spastic gait/ hemiparetic gait
is caused by lesion
interrupting the corticospinal
pathway.
• Usually arms are
flexed,adducted and internally
rotated and legs extended.
• Patient drags the foot and
scrapes the toes.
43.
44. Spastic-ataxic gait
• Features of both spasticity and ataxia,it usually results in a
spastic-ataxic gait.
• ‘jiggling’ or ‘bobing’ with tremulous,bouncing up and
down body movements.
• Causes-vit-B12 deficiency, multiple sclerosis,
HTLV/TSP, HIV associated vacuolar myelopathy,
Copper deficiency
45. Parkinsonian gait
• The gait is slow,stiff and
shuffling.as if patient is
trying to catch his own
centre of gravity
• Usually patient is
stooped,with head and
neck forward and knee
flexed;the upper extrimities
are flexed at the shoulders
elbow and wrist.
• Cog wheel rigidity
• Arm swing is decreased
46. • 60 year old male presented with gait disturbance in
the short shuffling festinant gait , bradykinesia ,
pillrolling tremors with rigidity. Patient was diagnosed
with parkinsons was started on levodopa with no
benefit .six months later he c/o about gait disturbance
with a feeling of right leg dragging with postural
imbalance, and difficulties in swallowing and
articulation.Toxic screen , gene testing for SCA was
negative. Patient cognitive function gradually
detetoriated.MRI revealed atrophy of cerebellum,
pons and middle cerebellar peduncle .(Positron
emission tomography (PET) was performed using 18F-
fluorodeoxyglucose (FDG), and showed decreased
cerebral glucose metabolism on the bilateral basal
ganglia, cerebellum, both parietal lobes, and left
posterior cingulate gyrus .
48. Multisystem atrophy
• Sporadic neurodegenerative disorder
• Pathology : cell loss , gliosis, glial cytoplasmic
inclusions( alpha synnuclein) in several CNS
structures
• Mutation of COQ2 gene
• Affects both men and women
• Main features : autonomic failure
,parkinsonism(80 % MSA P), cerebellar ataxia
(MSA c type)
49. Consensus statement for clinical
diagnosis of MSA
• Autonomic and urinary dysfuntion
1)Orthostatic hypotension (reduction in atleast 30
mmhg systolic bp or atleast 15 mm hg of
reduction of diastolic pressure after 3min of
standing )
2) Urinary incontinence (persistant, involuntary
partial or total bladder emptying , accompanied
by erectile dysfunction or both )
50. • MSA P associated Parkinsonism :
• Progressive akinesia and rigidity
• Jerky postural tremor and resting tremor
• Orofacial or craniocervical dystonia associated
with high pitched dysarthria
• Postural instability early in disease with
frequent falls
52. Disease progression
• Parkinsonism poorly responds to levodopa
• Cerebellar ataxia
• Early instablity and falls occur within 3 years
of disease onset
• Rapid progression of the disease ( wheelchair
bound despite dopaminergic treatment within
5 years of disease onset )
53. • 60 year old male presented with H/o
asymmetrical onset involuntary jerky
movements, bradykinesia , forgetfulness,
difficulty in swallowing, articulation.On
examination muscle bulk was normal with no
fasciculation .Tone of all limbs were increased
(R>L) with marked axial rigidity.Reflexes were
brisk with Right sided plantar flexor and left
equivocal.sensory examination was normal.
Patient had a stooped posture with short
shuffling gait. Patient was started on levodopa
but with no benefit . Patient developed repetitive
contraction of muscle with feeling of arm and
legs disconnected body.MRI was done revealed
atrophy of fronto temporal region.
56. Frontal gait disorder
• Also called gait apraxia where
there is loss of ability to use
legs properly in walking w/o
demonstrable sensory
impairment, weakness, or
incoordination.
• Usually occurs in frontal lobe
lesion ,NPH, Binswanger
disease, Pick’s disease.
• It is characterized by slightly
flexed posture, short,
shuffling steps and an
inability to integrate and
coordinate lower extremity
movement to accomplish
normal ambulation.
58. • 76 year old female came with C/O
forgetfullness , difficulty in remembering
names , decreased fluency had trouble in
performing learned motor skills with difficulty
in initiating gait (GAIT APRAXIA) On
examination there was decline in memory and
orientation with no sensory or motor
weakness.MRI and CT scan showing
predominant cortical and hippocampal
atrophy.
59. ALZHEIMER DISEASE
• RISK Factors : Old age / female sex / low level
of education / diabetes
• Mutations in gene encoding presinilin1 and
presinilin 2
• Characterised by memory impairment –
difficulty in naming , Aphasia is early and
prominent feature .
• Normal results on lab
• MRI shows predominant hippocampal atrophy
60. Steppage gait
Weakness of dorsiflexor- Tibialis anterior ,
The steps are regular and even, but the advancing foot
hangs with the toes pointing toward the ground.
high steppage gait in order to help the foot clear the
floor and avoid tripping.
Double tap
Causes: u/l foot drop - peroneal nerve palsy,
L5 radiculopathy.
polio, Multiple Sclerosis , GBS, Spinal disc
herniation
peroneal muscle atrophy, Peroneal nerve injury
polyneuropathy
61. Waddling /Trendelenburg gait
• During stance phase of gait cycle centre of
gravity is tranferred to the stance leg .
• Hip abducters stabilizes the pelvis.
• Abducter weakness of the stance leg causes
downward tilt of opposite pelvis to reduce
the load by deceasing the lever arm
• The patient walks with a broad base,with an
exaggerated rotation of pelvis that results in
a waddling gait.
. Causes-proximal muscle weakness, cushings
,polymyositis dermatomyosiitis
,LGMD,CDH, MND