1) The document discusses an approach to evaluating muscle weakness by differentiating true muscle weakness from fatigue or functional weakness. It provides a classification and diagnostic algorithm.
2) Key points in the evaluation include determining if weakness is objective or subjective, localized or generalized, and distinguishing upper motor neuron from lower motor neuron signs.
3) Differential diagnoses discussed include myopathies, motor neuron diseases, neuropathies, stroke, spinal cord lesions, multiple sclerosis, myasthenia gravis, and functional causes.
4) An algorithm is provided that approaches weakness by determining acuity and characteristics to guide appropriate testing and potential referrals.
Acute Transverse Myelitis
Blockage of the Spinal Cord’s Blood Supply
Cervical Spondylosis
Compression of the Spinal Cord
Hereditary Spastic Paraparesis
Subacute Combined Degeneration
Syrinx of the Spinal Cord and Brain Stem
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
A detailed description of benign paroxysmal positional vertigo (BPPV): the symptoms, causes, diagnosis, and treatment methods.For more information, please visit www.everydayhearing.com
Different types and categoroes of compressive myelopathy have been explained.
Their clinical findings, investgating features and radiological features have been discussed.
Acute Transverse Myelitis
Blockage of the Spinal Cord’s Blood Supply
Cervical Spondylosis
Compression of the Spinal Cord
Hereditary Spastic Paraparesis
Subacute Combined Degeneration
Syrinx of the Spinal Cord and Brain Stem
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
A detailed description of benign paroxysmal positional vertigo (BPPV): the symptoms, causes, diagnosis, and treatment methods.For more information, please visit www.everydayhearing.com
Different types and categoroes of compressive myelopathy have been explained.
Their clinical findings, investgating features and radiological features have been discussed.
This ppt nots specially for physiotherapy students this is for study purpose if you need this kind of short and brief study material keep following my website.. Education adda
Multiple sclerosis: Introduction, Risk Factors, Diagnosis and TreatmentEnriqueAlvarez93
Introduction about Multiple Sclerosis.
Risk factors affect to Multiple Sclerosis.
When to Suspect Multiple Sclerosis.
Evaluation and Diagnosis of Multiple Sclerosis.
How to treatment of Multiple Sclerosis.
Treatment of Multiple Sclerosis with Monoclonal Antibody.
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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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
2. Introduction:
• Weakness as professional/ medical term refer to symptom arise from
something wrong in muscle.
• In this situation very important to differentiate between weakness &
other confusing symptoms which mimic weakness as said by patient,
as fatigue.
• Weakness as mentioned before indicate the wrong is in the muscle,
either due to pathology with in muscle (myopathy), or pathology in its
motor nervous supply. So power of muscle will be decreased
according to MRC power rating system. This we name it, objective
muscle weakness, neuromuscular weakness, true muscle weakness
or clinical muscle weakness (i.e: clinically detectable muscle
weakness).
2
3. • Fatigue is subjective term reported by patient as weakness-like
complain felt after exercise but actually muscle power is normal, i.e:
no pathology in muscle or in its nerve supply. So fatigue is non-
objective muscle weakness, non-neuromuscular weakness,
functional muscle weakness or false muscle weakness.
Motor Nerve Supply
True Muscle Weakness
Wrong neither in
muscle nor in its
nerve supply
Functional
Muscle
weakness
[Myopathy]Muscle
3
4. Why approach to weakness is very
important?
• Because stroke enter in differential diagnosis of weakness which
severe condition & current stroke management mandates urgent
evaluation of unilateral limb weakness.
4
5. Classification by Algorithm-wise
Approach:
❑First of all keep in your mind the following helping questions:
• Mode of Onset & Duration:
oAcute: vascular, toxic & metabolic.
oChronic: neoplastic, infective, inflammatory, endocrine, degenerative
diseases.
• Course:
oWorse at onset then get regress later on: neurogenic cause: vascular.
oProgressive: neurogenic cause: neoplasm, degenerative & infective diseases.
oEpisodic: neurogenic cause: vascular.
oActivity dependent: NMJ cause: MG & muscular cause: myopathies.
5
6. • Co-morbidity: cardiopulmonary diseases, anaemia, infection,
malignancy & psychiatric illness. (as causes & risk factors of true
weakness & as a causes of functional weakness).
• Associated symptoms & signs:
oSymptoms of aetiologies & risk factors (cardiovascular, infections, endocrine,
malignancy, metabolic…etc).
oSymptoms help to differentiate between true & functional weakness
(constitutional, anemia, endocrine & positive drugs/ alcohol history).
oCortical dysfunction symptoms.
oSpinal lesion symptoms.
oSensory symptoms (distribution pattern of sensory loss help in localization
site of lesion).
oCranial nerves palsy & Bulbar symptoms (indicate brainstem involvement).
oAutonomic symptoms (bowel, bladder dysfunction & impotence): indicate
spinal cord/ nerves involvement below level of T1.
oIncrease intracranial pressure symptoms & signs.
oUMNL or LMNL signs.
6
8. Reviews:
Stroke:
•Most common cause of unilateral weakness.
•Patients typically present with sudden onset of the
complains.
•If persist < 3 hours , then it will resolve (TIA), while if
persist > 3 hours, then it will not resolve (true stroke).
•It can be cortical or spinal. Cortical is the common, so
“stroke” term alone usually refer to cortical one.
8
9. • Type of weakness in stroke is contralateral UMN hemiparesis/
hemiplegia.
• Usually associated with contralateral hemiparesthesia of all sensation
types, cortical dysfunction s/s, ibsilateral cranial nerves palsies
(suggesting brainstem involvement) producing what’s called crossed
hemiplegia or pseudobulbar palsy (UMN palsies of cranial nerves IX -
XII).
9
10. Space-occupying lesions (SOL):
•SOL, e.g. tumors, abscesses, chronic subdural
hematoma, can cause symptoms & signs mimicking
stroke but the onset is
typically more gradual
& progressive.
•There may be features
of raised ICP.
10
11. Spinal cord lesions:
•Above level of C5:
oHemicut: Ibsilateral UMN hemiparesis/ hemiplegia and deep
hemiparesthesia with contralateral superficial hemiparesthesia.
oComplete cut: UMN quadriparesis/ quadriplegia with bilateral loss
all sensation types.
N.B: If injury involve C3, C4 & C5, then patients will be died
(because these are root values of phrenic nerve).
•C5 to T1 (brachial plexus):
oHemicut: ibsilateral LMN hemiparesis/ hemiplegia and deep
hemiparesthesia with contralateral superficial hemiparesthesia in
upper limbs & ibsilateral UMN hemiparesis/ hemiplegia and deep
hemiparesthesia with contralateral superficial hemiparesthesia in
lower limbs.
11
12. o Complete Cut: bilateral LMN weakness with bilateral loss of all
sensation types in upper limbs & bilateral UMN weakness with
bilateral loss of all sensation types in lower limbs.
•T2 to L1:
oHemicut (Brown Sequard syndrome): ibsilateral UMN or LMN
monoparesis/ monoplegia in lower limb with ibsilateral deep
sensory loss & contralateral sensory loss take sensory level pattern
on trunk & autonomic dysfunction symptoms.
oComplete cut: UMN (spastic) paraparesis/ paraplegia or LMN
(flaccid) paraparesis/ paraplegia with or without sensory loss take
sensory level pattern on trunk & autonomic dysfunction
symptoms.
12
14. •Below L1 (Lumbosacral Plexus/ Cauda-Equina): always
LMN weakness in lower limbs unilaterally or bilaterally but not to
similar extent with sensory loss take “glove & stocking” pattern &
autonomic dysfunction symptoms.
14
16. Multiple Sclerosis (MS):
•Idiopathic inflammatory demyelinating disease of white
matter of the brain and spinal cord.
•Common in women between 20 – 40 years.
•Usually monosymptomatic.
•Characterized by relapsing & remitting course.
•Presented with motor, ocular sensory, cerebellar,
autonomic or cranial nerves abnormalities. The ocular
abnormality is the most common one.
•Can presented with almost any pattern of UMN limb
weakness, though paraparesis secondary to TM is the
most typical.
16
17. AHC Lesions; Motor Neuron Diseases (MND):
•It’s group of chronic degenerative diseases of unknown
etiology affecting the motor system only.
•Characterized by gradual onset and progressive weakness.
•Common in males > 50 years.
•Affect UMN or LMN or both. Can be presented with bulbar
symptoms.
•No sensory, cerebellar, autonomic or ocular abnormalities.
•It include: amyotrophic lateral sclerosis (ALS), lateral
sclerosis, progressive bulbar paralysis & spinal muscular
atrophy. The most important one is ALS.17
18. Peripheral nerve lesions:
•Cause LMN limbs weakness.
•Can be caused by:
o Metabolic causes: DM, Renal failure, Hypoglycemia.
o Inflammatory causes: GBS, Sarcoidosis, Chronic Inflammatory
Demyelinating Polyradiculoneuropathy (CIDP).
o Toxins: Botulism, Lead, Alcohol.
o Vasculitis: RA, PAN, Wegener’s granulomatosis.
o Drugs: INH, Phenytoin, Cisplatin.
o Congenital: Charcot Marie Tooth disease.
18
19. Guillain-barre Syndrome:
•It is acute ascending inflammatory
demyelinating polyneuropathy that is
autoimmune in nature.
•Can affect any age.
•Presentation is acute.
•H/O URTI, diarrhea, vaccination 2
weeks before the presentation.
•Symmetrical ascending weakness of
regressive course.
•Dyspnea is alarming sign.
19
20. NMJ lesions; Myasthenia Gravis (MG):
• Autoimmune neuromuscular disorder characterized by
fatigable LMN muscle weakness.
• Common in women between 20 – 40 years.
• Type of weakness is fatigable & of diurnal variation, i.e:
muscle power initially is normal then get weakens with
repeated activity to became true weakness at end of day.
• Associated with ocular & bulbar symptoms & tend to be
affected before limb muscles.
• Occur as relapsing & remitting course precipitated by
stress, infection, pregnancy & drugs.
20
22. Remember that:
•Muscle Power: preserved in patients with cachexia despite
advanced generalized muscle atrophy. In contrast, patients
with true muscle weakness due to myopathy have low
muscle power generally have normal muscle bulk at time of
presentation.
•Muscle Tenderness: usually not associated with one of the
causes of true muscle weakness, except for infectious
myopathies, certain drug- induced myopathies,
rhabdomyolysis, thyroid myopathy, and inherited metabolic
myopathies.
22
23. Diagnosis By
Algorithm-
wise
Approach:
Patient complain of
weakness
Is the weakness, true?
Is the true weakness is
strictly unilateral?
Unilateral weakness
Do blood
sugar test
This mean cortical stroke
excluded by far extent &
lesion is in spinal cord
(paraparesis/ paraplegia)
Is the onset, sudden?
Is it associated with features of acute limb ischemia
(pain, cold, pale, mottled skin & absent pulse)?
Request vascular surgeon
consultation
Urgent Spine MRI
• Cord compression
• Intrinsic spinal cord pathology
(Syringomyelia, TM, glioma, abscess)
Immobilize patient
& do cervical spine
image if there is
h/o trauma
Severe back pain + sparing of
proprioception & vibration?
Request neurosurgeon or
oncologist consultation
Spinal infarction
Are there UMN signs?
Is it associated with sensory
level & sphincter disturbance?
Is there MRI evidence
of myelopathy?
• Cord compression
• Intrinsic spinal cord pathology
(Syringomyelia, TM, glioma, abscess)
• SCDD (plasma
vitamin B12)
• Post-radiotherapy
myelopathy (Hx)
• MND; ALS (Hx &
Ex)
Bilateral intracranial
lesions: cerebral emboli/
metz, venous stroke,
demyelination/ MS (Hx &
Ex and brain image)
This is mean LMN signs
Are there sensory s/s?
Peripheral neuropathy
(distal weakness):
GBS (Hx, Ex, NCS, LP,
vital capacity monitor)
Refer to neurologist
CIDP (Hx, Ex, NCS, FBS,
HIV test, urinary
porphyrin, serum
protein
electrophoresis)
Refer to neurologist
Bilateral radiculopathy
(Hx, Ex, spinal cord
image)
Refer to neurologist
Otherwise:
• Ask about drugs/ alcohol Hx, family Hx of
charcot’s disease, social Hx of lead exposure
…etc
• Request following Ix: FBC, BS, U,E&C, ESR, CRP,
Ca, RF, TFT
Is there muscle
fatigability (fatigable/
post-exercise weakness)?
Tendon reflexes?
MG (Hx, Ex,
tensilon test,
EMG, anti-Ach
receptor AB,
thoracic CT)
LEMS (anti-
voltage-gated
calcium
channels AB,
EMG, screen
underlying
malignancy)
Proximal
weakness?
Myopathies
Hx: bedridden patient, drugs/
alcohol hx, past medical hx, past
surgical hx, h/o trauma …etc
Ix: FBC, U,E&C, ESR, CRP, BS, Ca,
RF, TFT, CK, EMG
Muscle Tenderness
• Infective myopathy (FBC, ESR, PCT)
• Some drugs induced myopathy (statin)
• Myositis; polymyositis, dermatomyositis
(anti-synthetase AB)
Other myopathies
• Insist on considering peripheral neuropathy, MND, mononeuritis multiplex,
myopathies, generalized weakness secondary to acute illness, functional weakness.
• Refer to neurologist if no cause identified.
Yes
Functional weakness (fatigue)
No
Yes
Yes
No
Yes
No
Yes
Yes
No
Yes
No
YesNo
YesNo
No
No
Yes
AbsentNormal
Yes
No
No
Is there weight Loss?
Is there pallor?
AnemiasIs the fatigue constant?
MGDrugs/ alcohol Hx?
• Alcohol
• Cocaine abuse
• Chronic aspirin
ingestion
• Anxiety
• Depression
• Fibromyalgia
• Aldosteronism
Is there fever?
• TB
• SBE
• Collagen diseases
• Other infections
Neurologic findings?
Is there Polyuria?
• Hyperthyroidism
• DM
• DI
• Hyperparathyroidism
• CKD
• Electrical disturbances
• Neoplasm
• Malnutrition
• Addison’s disease
• Cirrhosis
• Malabsorption syndrome
• CHF
• Parkinson’s disease
• Muscular dystrophy
• MND (ALS)
• MS
• Neuropathies
YesNo
No Yes
NoYes
+ve -ve
Yes No
-ve
+ve
NoYes
Is the onset, sudden?
Is it
painful?
Ischemia (compare pulse &
capillary refilling between 2 limbs)
Refer to vascular surgeon
Fracture (Hx of trauma & do X-ray)
Refer to orthopedist
Compartment syndrome (CK level
in blood)
Is duration > 3 hours?
Stroke TIA
Are there seizure,
evidence of increased
ICP, cortical dysfunction
or CNS infection?
• SOL
• Meningoencephalitis
(fever, purpuric skin
rashes & meningeal
irritation signs)
• LP
• Neuroimage
Are there UMN signs?Is there contralateral sensory loss?Unilateral spinal cord lesionsMRI Spine
• Ipsilateral sensory loss: SOL, stroke, MS
• Normal sensation: MND
Is signs are referable to
single nerve root/ single
nerve?
Radiculopathy or mononeuropathy
• Insist on considering plexopathy, multi-root compression,
MND, stroke, migraine, functional weakness.
• Refer to neurologist if no cause identified.
Yes
No
Yes
Yes
No
Yes
No
YesYes
No
No
No
Yes
MRI Spine
Yes
No
No
Yes
No
Motor Cortex
Spinal Cord
Peripheral Nerves
NMJ
Muscle
Bilateral True Weakness
Unilateral True Weakness
Functional Weakness
23
24. Sources:
• Macleod's Clinical Diagnosis 2nd Ed (2013)
• Approach to Internal Medicine 4th Ed (2015)
• Algorithmic Diagnosis of Symptoms and Signs 4th Ed (2017)
• Toronto Notes 34th Ed (2018)
• Ain-Shams University Internal Medicine curriculum (2014)
• Decision Making in Medicine 3rd Ed (2010)
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