This document discusses the anatomy, functions, and clinical presentations of lesions involving the frontal lobe, including the motor cortex, prefrontal cortex, and their roles in executive function, social behavior, language, and more. Specific tests are described to evaluate functions like motor control, language, problem-solving, and emotional regulation that are mediated by the frontal lobe. A variety of clinical syndromes can result from frontal lobe lesions depending on the location and extent of the damage.
Understanding the encoding of memory and its retrieval is a complex task. The neurobiological correlates of memory have been summarised in this presentation for easy understanding of students.
The association of neuropsychiatric disorders with cerebrovascular disease has been recognized by clinicians for over 100 years. Disease of the vascular system contribute greatly to the sum total of psychiatric disability, chiefly in the elderly population, mainly as a result of stroke, cerebrovascular accidents & subarachnoid haemorrhage.
Understanding the encoding of memory and its retrieval is a complex task. The neurobiological correlates of memory have been summarised in this presentation for easy understanding of students.
The association of neuropsychiatric disorders with cerebrovascular disease has been recognized by clinicians for over 100 years. Disease of the vascular system contribute greatly to the sum total of psychiatric disability, chiefly in the elderly population, mainly as a result of stroke, cerebrovascular accidents & subarachnoid haemorrhage.
This is a medical grade presentation on Neurology- Frontal lobe clinical anatomy, physiology, functions, diseases. Can be used as last minute revision and notes on frontal lobe with easy pointers to remember.
Traumatic Brain Injury to temporal lobe and cognitive rehabilitationRavi Soni
This presentation briefs you about temporal lobe basic anatomy, Structures, functions, Mechanisms of Temporal lobe Injury and Cognitive rehabilitation strategies for temporal lobe deficits
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
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
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
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.
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
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!
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.
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.
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.
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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.
3. Cerebral Features:
• Gyri – Elevated ridges “winding” around the brain.
• Sulci – Small grooves dividing the gyri
– Central Sulcus – Divides the Frontal Lobe from the Parietal Lobe
• Fissures – Deep grooves, generally dividing large
regions/lobes of the brain
– Longitudinal Fissure – Divides the two Cerebral Hemispheres
– Transverse Fissure – Separates the Cerebrum from the
Cerebellum
– Sylvian/Lateral Fissure – Divides the Temporal Lobe from the
Frontal and Parietal Lobes
4. Specific Sulci/Fissures:
Central Sulcus
Longitudinal Fissure
Sylvian/Lateral
Fissure
Transverse Fissure
* Note: Occasionally, the Insula is considered the fifth lobe. It is located deep
to the Temporal Lobe.
5. Cerebrum - The largest division of the brain. It is
divided into two hemispheres, each of which is divided
into four lobes
• Cerebral Cortex - The outermost layer of gray matter
making up the superficial aspect of the cerebrum
6. Functional Frontal Lobe Anatomy
• Phylogenetically youngest
part of brain
• Located deep to the frontal
bone of the skull
• Largest of all lobes
– SA: ~1/3 / hemisphere
• 3 major areas in each lobe
– Dorsolateral aspect
– Medial aspect
– Inferior orbital aspect
7. Frontal lobe
• Motor cortex Prefrontal cortex
– Primary motor – Dorsolateral
– Premotor – Medial
– Supplementary motor – Orbitofrontal
– Frontal eye field
– Broca’s speech area
8. Functional Frontal Lobe Anatomy
Premotor area Primary motor area
BA 6,8 BA 4
Central sulcus
Supplementary
motor area
(medially BA 6)
Frontal eye field
BA 8
Prefrontal cortex
BA 9, 10, 11, 12
Lateral sulcus/
Sylvian fissure
Motor speech
area of Broca
BA 44, 45
9. • Prefrontal area consist of paralimbic (anterior
cingulate gyrus & posterior orbitofrontal) and high
order association cortex (dorsolateral convexity &
anteromedial surface)
• This area was considered “silent”
Prefrontal
cortex
10. Functional regions of the left frontal lobe functional regions of the right frontal lobe
(lateral view) (medial view)
11. Motor Cortex
• Primary motor cortex BA 4
– Input: thalamus, BG, sensory,
premotor
– Output: motor fibers to
brainstem and spinal cord
– Function: executes design into
movement
– Lesions: tone (spasticity);
power; fine motor function
on contra lateral side
12. • Bedside test :-
• Motor strength of hand grip
• Motor speed on finger tapping
• Diagnostically, poor performances suggest local
lesions such as vascular or neoplastic pathology, or a
generalized lesion such as a degenerative disease.
13. Motor Cortex
• Premotor cortex BA 6
– Input: thalamus, BG, sensory cortex
– Output: primary motor cortex
– Function: sensorimotor integration, stores
motor programs; controls coarse postural
movements
Lesions: moderate weakness in proximal muscles on
contralateral side, spasticity, grasp reflex,
buccofacial apraxia, inability to make use of sensory
feedback in the performance of smooth movements
14. • Bedside test :-
• 1. Sensorimotor abilities are tested by asking the
patient touch each finger to the thumb in succession
as rapidly as possible (Watch for speed and dexterity)
• 2. Apraxia can be tested by asking the patient to
"blow a kiss" and to demonstrate the use of a shovel.
• Poor performance carries the diagnostic implications
15. Motor Cortex
• Supplementary motor area medial aspect of BA 6
– Input: cingulate gyrus, thalamus, sensory & prefrontal
cortex
– Output: premotor, primary motor
• Function: involved in motivated behavior, initiation
and goal directed behavior, intentional preparation
for movement; procedural memory
• Lesions: transient transcortical motor aphasia
(mutism), impairment in motor initiation
(akinesis); impaired rapid alternating movements,
grasp reflex, alien hand syndrome
16. Motor Cortex
• Frontal eye fields BA 8 with some area of 9 & 6
– Input: parietal / temporal (what is target);
posterior / parietal cortex (where is target)
– Output: caudate; superior colliculus;
paramedian pontine reticular formation
– Function: selects target and commands
movement (saccades)
– Lesion: eyes deviate ipsilaterally with
destructive lesion and contralaterally with
irritating lesions
17. • Bedside test:-
• 1. Ask the patient to follow the movement of a finger
from left to right and up and down.
• 2. Ask the patient to look from left to right, up and
down (with no finger to follow).
• Note inability to move or jerky movement.
18. Motor Cortex
• Broca’s speech area BA 44, 45
– Input: wernicke’s area
– Output: primary motor cortex
– Function: speech production (dominant hemisphere);
emotional melodic component of speech (non-dominant)
– Lesions: motor aphasia; dysprosody (monotonus speech)
– Speech is sparse, slow, hesitant, disturbance of rhythm and
articulation, difficulty in word finding, wrong words are
chosen & often mispronounced, perseveration,
agrammatism
– Pt recognize his mistakes & tries to correct them but
becomes impatient
– Phrase length is small :- telegraphic language
– Writing is also affected with speech, but comprehension is
preserved
19. Prefrontal Cortex
• Orbital prefrontal cortex BA 10 & 11
– Connections: temporal, parietal, thalamus, GP,
caudate, SN, insula, amygdala
– Part of limbic system
• Function: It mediates empathic, civil and socially
appropriate behavior, emotional input, arousal,
suppression of distracting signals
– Lesions: emotional lability, disinhibition, distractibility,
‘hyperkinesis’
• Much of the personality change described in cases of
frontal lobe injury is due to lesions in this area
20. Bedside tests:
• 1. Does the patient dress or behave in a way which
suggests lack of concern with the feelings of others
or without concern to accepted social customs.
• 2. Test sense of smell - coffee, cloves etc.
• 3. Go/no-go Test- The patient is asked to make a
response to one signal (the Go signal) and not to
respond to another signal (the no-go signal)
• 4. The Stroop Test - Examines the ability of the
patient to inhibit responses
22. Prefrontal Cortex
• Dorsolateral prefrontal cortex BA 9 and the lateral aspect
of 10 and most of area 46
– Connections: motor / sensory convergence areas,
thalamus, GP, caudate, SN
• Functions: executive functioning include the integration
of sensory information, the generation of a range of
response alternatives to environmental challenges, the
selection of the most appropriate response,
maintenance of task set, sequential ordering of data,
self-evaluation of performance and the selection of a
replacement responses if the first applied response fails
monitors and adjusts behavior using ‘working memory’
– Lesions: executive function deficit, apathy,
aspontaneity and impoverished & stereotyped
thought process
23. Bedside tests:-
• 1. Is the patient able to make an appointment and
arrive on time?
• 2. Is the patient able to give a coherent account of
current problems
• Digit span, days of the week or months of the year
backwards
• Controlled oral word association test (COWAT): the
patient is asked to
• FAS verbal fluency test - produce as many words as
possible, in one minute, starting with F, then A, then S
24. • Alternating hand sequences :- one hand is placed palm
upwards and the other is place palm downwards, and
the patient is then asked to reverse these positions as
rapidly as possible or
• Patient taps twice with one fist and once with the
other, then after the rhythm is established, the patient
is asked to change over the number of beats
• Patients with frontal lobe deficits usually perform
poorly on these tests, often unable to follow relatively
simple instructions
25. • Formal neuropsychological tests may be necessary
where uncertainty remains
• Commonly employed tests include Controlled Oral
Word Association Test (Benton, 1968) and the
Wisconsin Card Sorting Tests (Heaton, 1985)
Wisconsin Card Sorting Test
“Please sort the 60 cards under the 4 samples (stimulus cards).
I won‟t tell you the rule, but I will announce every mistake.
The rule will change after 10 correct placements.”
26. Neurotransmitters
• Dopaminergic tracts
– Origin: ventral tegmental area in midbrain
– Projections: prefrontal cortex (mesocortical tract)
and to limbic system (mesolimbic tract)
– Function: reward, motivation, spontaneity, arousal
27. Neurotransmitters
• Norepinephrine tracts
– Origin: locus ceruleus in brainstem and lateral
brainstem tegmentum
– Projections: anterior cortex
– Functions: alertness, arousal, cognitive processing
of somatosensory information
28. Neurotransmitters
• Serotonergic tracts
– Origin: raphe nuclei in brainstem
– Projections: number of forebrain structures
– Function: minor role in prefrontal cortex; sleep,
mood, anxiety, feeding
29. • PREFRONTAL LESIONS cause prominent personality
changes without loss of general intelligence, motor,
sensory or memory functions – FRONTAL LOBE
SYNDROME
Frontal lobe syndrome
Features not unique to frontal
lobe pathology
Lack of one to one
correspondence b/w behavior &
location of lesion
Executive syndrome
(Baddely & Wilson)
30. • A 45 year old man with b/l prefrontal strokes was
found to have
– Normal neurological examination
– Slightly flattened affect
– Lack of spontaneity, mental slowness
– Increased left sided motor tone
– Neuropsychological testing – normal intelligence &
memory
– Demoted at his managerial jobs d/t ineffective work habits
– Unable to adequately supervise children
– Often lost his temper
– Inattention
– Bad judgment
31. • CLINICAL PICTURE : varies among pts.
• Individual features depends on
• Nature & time course of pathological process
• Lateralization
• Localization
• Extent of involvement among subcortical & callosal
fibers
• Secondary effect of raised ICT
• Kliest first suggested that components of frontal lobe
syndrome may be related to specific regional
involvement
32. • Orbital lesions cause : Disinhibition, failure to appreciate
consequences of one’s action, euphoria (effect on
personality & social behavior)
• Lesions of dorsolateral convexity cause : Apathy,
aspontaneity, impoverished & stereotyped thought
process
• Left prefrontal injury : loss of executive & planning
function, depression,
• When supplementary/ premotor area affected :
transcortical motor aphasia, impairment of rapid skilled
manual movements
• Right prefrontal injury : left sided extinction & neglect,
blunted or labile affect, impersistence, disinhibition,
confabulation, alien hand sign
33. • Patients with classical frontal lobe syndrome usually have
b/l lesions encompassing both orbital & lateral cortex
• Negative symptoms :
• Lack of initiative & spontaneity
• General diminution of motor activity (sluggish response)
• Task are left unfinished
• New initiatives are rarely undertaken
• Capacity to function independently in life is affected
• Cognition & intellect may remain unaffected
• Yet when vigorously urged or constrained by structural
situation pt may function quite well
34. • Other pts may show positive symptoms
• Restless
• Hyperactive yet lack of goal directed behavior
• Mild euphoria
• Tendency to joke/pun
• State of excitement, pressured speech
• Overfamilarity
• Outburst of irritability
• Such changes are rarely sustained and when left to
themselves these pts become inert & apathetic
35. • Social awareness & behavior
• Less concerned with consequences of his acts
• Loss of social graces
• Coarsening of personality
• Lack of normal adult tact & restraints
• Little concern about his future
• Fails to plan ahead, to carry out ideas
• Sexual disinhibition
• Pt usually has little insight into the changes
36. • Inability to plan & execute multistepped behavior is
hallmark of prefrontal lesions
• Can manage simple one or two step command
• Evaluated by asking the pt & spouse, do things get
started but not completed?
• Ask pt about planning a vacation, changing a tyre.
• Test of sequential motor & visual patterns
– Reciprocal coordination test
– Sequential motor test
– Visual pattern completion task
37. • Wisconsin card sorting test : shift cognition sets
• Perseveration is another symptom of frontal lobe
disorder but not pathognomic
• Concrete thinking or lack of abstraction
– Proverb test
– Similarity test
Bifrontal lesions
Bad judgment resulting
from deficits affecting Lack of awareness, Family,
Planning & carrying out attentional deficits, relation,
multistepped behavior, understanding, occupation
adaptation to new sensitivity & problems
situation, understanding communication skills
& reacting social cues
38. • Abulia : Poverty of thought action & emotion is
common with large midline and b/l dorsofrontal
lesion
• Abulia is characterized by loss of spontaneity & will
power
• They comprehend the question, hesitate, delay
respond, seem to ignore or give yes – no answer
• Severely abulic pt do not speak unless spoken, do not
move unless they are hungry or ready to void & may
be incontinent
• Tidal waves of emotional & motor behavior (brief
rage, irritability, hyperactivity) may emerge from
tranquil sea of abulia (placid, apathetic, disinterested)
• Perseveration v/s abulia :- Random A test.
39. • Classical case reports
• The Case of Phineas Gage (Harlow 1868)
tamping iron blown through
skull: L frontal brain injury
excellent physical recovery
dramatic personality change:
„no longer Gage‟:stubborn,
lacked in consideration for
others, unreliable, lacking in
social skills, had profane
speech, failed to execute his
plans
40. • Utilisation behavior (Lhermitte 1986)
• Observed pt with frontal lobe lesion in complex
everyday life situation
• He noted lack of personal autonomy with an excessive
dependence on social & physical environment
(environmental dependency syndrome)
• Decisions of pts actions were not made by themselves
• Social & physical environments issue the order to use
them even the pt has neither idea or nor intend to use
them
41. Diseases Commonly Associated With Frontal
Lobe Lesions
• Traumatic brain injury
– Gunshot wound
– Closed head injury
– Contusions and intracerebral hematomas
• Vascular disease
– Common cause especially in elderly
– ACA territory infarction
• Damage to medial frontal area
– MCA territory
• Dorsolateral frontal lobe
– ACom aneurysm rupture
• Personality change, emotional disturbance
44. Schizophrenia
• Symptoms can be aggregated in 3 broad clusters (Liddle 1987)
1. Psychomotor poverty syndrome
Affecting speech & movement, blunting of affect
Decreased rCBF in left prefrontal & parietal cortex
45. 2. Reality distortion syndrome
Positive symptoms hallucinations & delusions
Increase rCBF in left parahippocampal gyrus & contiguous
area
3. Disorganization syndrome
Thought disorder & inappropriate affect
Increase resting rCBF in anterior cingulate region
46. Frontal lobe & depression
• Depression is often a realistic reaction to misfortunes
• Requires the cognitive capacity to appreciate and thus feel
depressed
• In consequence :
• Area of the brain mediating the depression may become
excessively active
• Whereas yet another region of the cerebrum which is
expressing the depression may become underactive
• Right frontal lobe demonstrated increased activity in
response to negative moods
• Not only reductions in left frontal activity, but injuries to
the left frontal lobe have been consistently associated with
depression, "psycho-motor" retardation, apathy, irritability,
and blunted mental functioning
47. Frontal lobe & ADHD
• Executive functions of frontal cortex include:
– Problem solving
– Attention
– Reasoning
– Planning
• ADHD suffers usually have deficits in these functions
• Right frontal lobe is smaller in children with ADHD
• Problems in the circuit between three regions are the
underlying mechanisms that cause ADHD symptoms
1. Prefrontal cortex (command center)
2. Caudate nucleus
3. Globus pallidus
48. Frontal lobe & OCD
• OCD could be due to abnormalities of the frontal
lobe, basal ganglia, and cingulum
• OCD is caused by problems in communication
between the frontal lobe and basal ganglia
• On PET Scan, OCD pt burned energy more quickly in
the frontal lobe and cingulate pathway
• Abnormally low levels of serotonin found in people
with OCD
49. Frontal lobe & alcoholism
• Prefrontal cortex has been linked to impulse control
because damage to this region of the brain can lead
to loss of inhibitions
• Two neurotransmitters, gamma-amino butyric acid
(GABA) and dopamine are responsible for the loss of
impulse control in those who consume alcohol
• Alcohol increases the amount of dopamine release
and enhances the normal feeling of pleasure
• Alcohol co binds with GABA to GABA receptor and
hyperpolarize the post synaptic neuron, so ability of
the neurons in the frontal lobes to inhibit socially
unacceptable behavior is reduced
50. Frontal lobe epilepsy
• IInd most common type of epilepsy
• Brief recurring seizures often while pt is sleeping
• 2 forms :-
• Simple partial seizures : does not affect awareness & memory
• Complex partial seizures : affects awareness & memory
• Symptoms :-
• Physical/emotional aura of tingling, numbness, tension
• Fear expressed on face
• Tonic posturing & clonic movements
• Often misdiagnosed as psychogenic seizures
• More specific symptoms depends on area of frontal cortex
involved
51. • Supplementary motor area : somatosensory aura precedes tonic
posturing which is u/l, asymmetrical
• Motor symptoms :- facial grimacing, complex automatism like
kicking, pelvic thrusting
• Vocal symptoms :- laughing, yelling or speech arrest
• Primary motor cortex : jacksonian seizures that spread to
adjacent area, often triggers to IInd round of seizures
• Usually tonic, myoclonic movements with speech arrest
• Medial frontal, Cingulate gyrus, Orbitofrontal, Frontopolar region :
• Short repetitive thrashing, pedaling, thrusting, laughing,
screaming, crying
• Motor symptoms are accompanied by emotional feelings &
viscerosensory symptoms
• Often misdiagnosed as psychological seizures
52. • Dorsolateral cortex : tonic posturing & clonic movements
• c/l head turning & eye deviation
• Operculum : symptoms involve head & digestive tract as
swallowing, mastication
• Person is fearful, clonic facial movements & speech is often
arrested
• Diagnosis : EEG, MRI
• Treatment :
• Medical : anticonvulsants as carbamazepine, phenytoin,
gabapentine, lamotrigine, topiramate etc.
• Surgical : frontal lobectomy, multiple subpial transections,
gamma knife radiosurgery, vagus nerve stimulator
• Diet : ketogenic diet, high fat & low carbohydrate
53. Frontal lobe & memory
• Focal frontal injury does not produce a severe
amnesic disorder
• It can cause more subtle, yet definable, memory
deficits in form of an impairment in the control of
memory
• Prefrontal cortex appears to be crucial for the
monitoring and control of memory processes, both
at the time of encoding and at the time of retrieval
• Significant impairment was observed on tests of free
recall (80% of studies), cued recall (50% of studies)
and even on tests of recognition (8% of studies)
54. To conclude
• Frontal lobe forms about 1/3 part of each cerebral
hemisphere
• Phylogenetically newest part
• Previously considered silent brain, but now found to
produce variety of symptoms
• 2 major parts
• (a) precentral/motor cortex :- planning, execution &
control of c/l body movements
• (b) prefrontal cortex :- emotion control center & home of
our personality
• Bilateral prefrontal cortex lesion leads to frontal lobe
sydrome
55. To conclude
• Left prefrontal cortex lesion :- psuedodepressive type
• Right prefrontal cortex lesion :- psuedopsychotic type
• Inability to plan & execute multistepped behavior is
hallmark of prefrontal lesion
• Frontal lobe functions are deranged in schizophrenia,
depression, ADHD, OCD, antisocial personality disorder,
alcoholism etc.
• Frontal lobe epilepsy is often misdiagnosed as psychogenic
seizures
• prefrontal cortex is crucial for control of memory during
encoding & recall