a.

Anosognosia
- Anosognosia is a neurological condition characterized by a person's inability to recognize or acknowledge
their own illness, disability, or impairment. It is most commonly associated with certain brain disorders,
such as stroke, traumatic brain injury, Alzheimer's disease, and certain psychiatric conditions like
schizophrenia.
- Individuals with anosognosia may be completely unaware of their condition or may have a distorted
perception of their abilities or disabilities. For example, a person with left-sided paralysis resulting from a
stroke may deny or be unaware of their paralysis and may even attempt to use the affected limb, despite
its inability to function.
- It's worth noting that anosognosia should not be confused with denial, which is a psychological defense
mechanism where individuals consciously reject or refuse to accept a reality or diagnosis. Anosognosia is
a genuine lack of awareness or insight into one's condition due to neurological factors.
b. Spastic
c. Asterixis
- Asterixis, also known as "flapping tremor" or "liver flap," is a neurological sign characterized by a rapid,
non-rhythmic, and involuntary flapping movement of the hands or wrists when the arms are extended and
the hands are dorsiflexed (bent backward at the wrist). This movement resembles a bird flapping its wings.
- Asterixis is commonly associated with liver disease, particularly hepatic encephalopathy, which is a
condition characterized by impaired liver function leading to the buildup of toxins in the bloodstream.
However, it can also occur in other neurological conditions, such as uremic encephalopathy (caused by
kidney failure), certain metabolic disorders, carbon dioxide retention, and drug intoxication.
d. Rigidity
- Rigidity refers to a stiffness or resistance to movement in muscles. It is often associated with increased
muscle tone and is commonly seen in conditions such as Parkinson's disease. Rigidity can be described
as either "cogwheel" (intermittent resistance to movement) or "lead pipe" (continuous resistance).
e. Hemiplegia
- Hemiplegia is a paralysis or weakness affecting one side of the body, typically resulting from damage or
injury to the brain or spinal cord on the opposite side. It involves the loss of motor function on the affected
side, including both the arm and leg.
f. Hemiparesis
- Hemiparesis is similar to hemiplegia but refers to partial paralysis or weakness affecting one side of the
body. In hemiparesis, there is a noticeable decrease in strength and control of movement on the affected
side.
g. Paraplegia
- Paraplegia refers to paralysis or loss of motor and sensory function in the lower limbs and lower part of the
trunk. It typically occurs due to spinal cord injury or disease below the neck level.
h. Quadriparesis
- Quadriparesis is a condition characterized by weakness or partial paralysis of all four limbs (both arms and
both legs), usually caused by a spinal cord injury or certain neurological disorders.
i. Aphasia
- Aphasia refers to a language disorder that affects a person's ability to speak, understand, read, or write. It
can result from brain damage, such as a stroke or traumatic brain injury, and may vary in severity from mild
difficulty finding words to complete loss of language function.
j. Ataxia
- Ataxia is a lack of coordination and control of voluntary movements. It can manifest as unsteady gait,
clumsiness, and difficulty with fine motor tasks. Ataxia can be caused by various conditions, including
cerebellar dysfunction or damage to the sensory pathways that coordinate movement.
k. Dysmetria
- Dysmetria refers to a difficulty in judging distances or range of movement, resulting in overreaching or
underreaching when attempting to perform coordinated movements. It is commonly observed in cerebellar
disorders.
l. Dysdiadochokinesia
- Dysdiadochokinesia refers to the impaired ability to perform rapid alternating movements, such as rapidly
pronating and supinating the hands. It is a characteristic finding in cerebellar dysfunction.
m. Paratonia
- Paratonia, also known as gegenhalten, is a form of resistance to passive movement characterized by
involuntary muscle contraction in response to an examiner's attempt to move a limb. It is commonly seen
in individuals with cognitive impairment or neurological conditions.
n. Myoclonus
- Myoclonus is a sudden, brief, involuntary muscle contraction or jerk. It can affect individual muscles or
involve multiple muscle groups. Myoclonus can occur spontaneously or be triggered by certain stimuli and
may be seen in various neurological disorders.
o. Stereognosia
- Stereognosia refers to the ability to recognize objects by touch and manipulation without visual input. It
involves integrating sensory information from touch, proprioception, and tactile memory to identify objects.
p. Graphestesia
- Graphesthesia is the ability to recognize and interpret numbers, letters, or other symbols traced or drawn
on the skin without visual input. It is a form of tactile perception that relies on the integration of touch and
somatosensory information.
2. Formation of CSF
- CSF Formation in the Choroid Plexus: CSF is primarily formed in specialized structures called choroid
plexuses, which are located in the ventricles of the brain. The choroid plexuses consist of tufts of
capillaries covered by a layer of ependymal cells. Blood flows through these capillaries, and through a
process called filtration, fluid and solutes are pushed out of the capillaries and into the ependymal cells.
- Secretion of CSF: Within the ependymal cells, there are transport mechanisms that actively secrete certain
substances from the blood into the ventricles. These substances include water, electrolytes (such as
sodium, potassium, and chloride ions), glucose, and various molecules like neurotransmitters. This active
secretion contributes to the composition of CSF.
3. What areas of the brain are not protected by the BBB?
The blood-brain barrier (BBB) is a specialized barrier formed by the endothelial cells lining the blood vessels in
the brain. Its primary function is to regulate the movement of substances from the bloodstream into the
brain to maintain a stable and protected environment. While the BBB is highly effective in restricting the
passage of many substances, there are some areas in the brain that have a reduced or incomplete BBB,
allowing for greater permeability. These areas include:
1. Area Postrema: The area postrema is located in the medulla oblongata of the brainstem, specifically within
the fourth ventricle. It plays a role in detecting toxins in the bloodstream and triggering the initiation of the
vomiting reflex. The area postrema has a weak blood-brain barrier, allowing certain substances to directly
affect it and induce vomiting.
2. Pineal Gland: The pineal gland, situated in the epithalamus, is responsible for producing melatonin, a
hormone involved in regulating sleep-wake cycles. The pineal gland has fenestrated capillaries, which
means they have small pores that allow for greater permeability of substances.
3. Median Eminence: The median eminence is a region at the base of the hypothalamus, where the
hypothalamus connects with the pituitary gland. It acts as a bridge between the brain and the pituitary
gland, which controls the release of various hormones. The median eminence has a less restrictive
blood-brain barrier, allowing certain substances and hormones to cross into the pituitary gland.
4. Neurohypophysis (Posterior Pituitary): The posterior pituitary, also known as the neurohypophysis, is a part
of the pituitary gland. It is responsible for releasing hormones such as oxytocin and vasopressin. The blood
vessels within the posterior pituitary have fenestrations, allowing for easier passage of hormones.

It's important to note that while these areas have a relatively less stringent blood-brain barrier, they still
possess some level of protection. The permeability in these regions serves specific physiological functions
while maintaining the overall integrity of the brain's environment.

Understanding the areas of the brain that have reduced or incomplete blood-brain barrier (BBB) protection is
medically important for several reasons:

1. Drug Delivery: Knowledge of areas with compromised BBB helps in the development of therapeutic
strategies. Some medications may have difficulty crossing the intact BBB to reach the desired target within
the brain. Identifying areas with relatively easier drug penetration allows for the development of specific
drug delivery approaches to treat conditions affecting those regions.
2. Disease Pathology: Certain neurological conditions, such as brain tumors, infections, or neurodegenerative
diseases, can affect areas with weakened BBB integrity. Understanding which areas are more vulnerable
can provide insights into the pathogenesis and progression of these conditions.
3. Neurotoxicity and Neuroinflammation: The areas with reduced BBB protection may be more susceptible to
the entry of toxins, pathogens, or immune cells into the brain. This knowledge is crucial for understanding
the mechanisms of neurotoxicity and neuroinflammation in specific brain regions.
4. Hormone Regulation: The areas with less restrictive BBB, such as the pineal gland, median eminence, and
posterior pituitary, are involved in hormone regulation. Understanding the permeability of these regions
helps in studying hormonal disorders and developing appropriate treatment strategies.
5. Brain Imaging Interpretation: In medical imaging, knowledge of regions with altered BBB integrity aids in the
interpretation of imaging findings. Contrast agents used in imaging techniques can indicate areas of BBB
disruption, suggesting potential pathology or assisting in the localization of lesions.
6. Development of Therapies: The identification of areas with compromised BBB may guide the development
of novel therapeutic approaches. Strategies such as targeted drug delivery, gene therapy, or immune
modulation can be tailored to these specific regions to enhance treatment efficacy.

4. Circle of WIllis
Collateral Circulation: The Circle of Willis serves as a vital collateral circulation system. It is formed by the
merging of several major arteries at the base of the brain, including the two internal carotid arteries
(supplying the anterior circulation) and the two vertebral arteries (supplying the posterior circulation). This
interconnected network allows for alternative routes for blood flow if there is an occlusion or stenosis in
one of the major arteries supplying the brain. In such situations, blood can be rerouted through the Circle
of Willis to ensure continuous perfusion to critical brain regions, reducing the risk of ischemic damage.
Compensation for Variations: The Circle of Willis exhibits natural anatomical variations in its structure and
completeness among individuals. Understanding these variations is important because it determines the
effectiveness of collateral circulation. For example, if one major artery is compromised, the presence of a
well-developed Circle of Willis with adequate connections can compensate for the reduced blood flow by
redirecting it through alternative pathways.
Ischemic Stroke Protection: The Circle of Willis plays a crucial role in protecting the brain against ischemic
strokes, which occur due to blockage or reduced blood flow to a particular region of the brain. In cases
where a major artery supplying the brain becomes occluded (e.g., due to an embolus or atherosclerosis),
the Circle of Willis can provide a backup supply of blood. This collateral flow helps maintain perfusion to
affected brain regions and reduces the risk of tissue damage and neurological deficits associated with
ischemic strokes.
Hemodynamic Stability: The Circle of Willis helps equalize blood flow and pressure between the cerebral
hemispheres and the anterior and posterior regions of the brain. This ensures a balanced supply of blood
and oxygen to different areas, promoting optimal brain function. It helps maintain stable cerebral perfusion
and prevents significant disparities in blood flow that could lead to ischemia or compromised brain function.
Clinical Relevance: Understanding the anatomy and function of the Circle of Willis is crucial for clinical
practice. Knowledge of its variations and potential limitations in collateral circulation aids in interpreting
diagnostic imaging studies, planning surgical interventions, and assessing the risk of ischemic events in
patients with vascular diseases or those undergoing certain procedures.

5. Where is the lesion

G. Electric Sensation radiating to the distal extremities
- This symptom could be indicative of a peripheral nerve pathology, such as peripheral neuropathy. The
lesion is likely to be located in the peripheral nerves, possibly in the distal segments.
H. Diffuse distal sensory/motor deficit
- A diffuse distal sensory/motor deficit suggests a possible involvement of peripheral nerves or nerve roots.
The lesion may be located in the peripheral nerves, nerve roots, or the distal segments of the spinal cord.
I. Diffuse Proximal motor weakness
- Diffuse proximal motor weakness may suggest an issue with the motor pathways or muscles. The lesion
could be located in the motor cortex, subcortical white matter, or spinal cord.
J. Fluctuating Proximal Motor Weakness
- Fluctuating proximal motor weakness may be associated with a neuromuscular junction disorder, such as
myasthenia gravis. The lesion may be at the neuromuscular junction itself.
K. Aphasia, Agnosia, Apraxia
- The presence of aphasia, agnosia (difficulty recognizing objects or people), and apraxia (difficulty with
purposeful movements) suggests involvement of the dominant hemisphere of the brain. The lesion is likely
to be located in the language areas, such as Broca's area or Wernicke's area, along with other associated
cortical regions.
L. Left Face & Body Hemianesthesia
- Left face and body hemianesthesia, which is the loss of sensation on the left side of the face and body,
typically indicates a lesion in the right hemisphere of the brain. The lesion is likely to be located in the
somatosensory cortex or the sensory pathways on the right side of the brain.
6. What is the lesion?
7. 5 levels of sensorium
8. Enumerate the 7 types of Aphasia and what physical examination modalities to use to differentiate
them
A. Broca's Aphasia (Expressive Aphasia):
Fluency: Non-fluent speech characterized by slow, effortful, and halting production.
Repetition: Repetition is typically impaired or labored.
Comprehension: Comprehension is relatively preserved, although there may be difficulty with complex
sentence structures and comprehension of syntactic relationships.
B. Wernicke's Aphasia (Receptive Aphasia):
Fluency: Fluent speech with normal or increased rate, but it may lack meaningful content and be marked by
neologisms (made-up words) and paraphasias (word substitutions).
Repetition: Repetition is typically impaired, with difficulty reproducing phrases accurately.
Comprehension: Comprehension is significantly impaired, making it challenging to understand spoken or
written language and follow commands.
C. Global Aphasia:
Fluency: Severely limited speech output, often consisting of only a few words or utterances.
Repetition: Repetition is severely impaired or absent.
Comprehension: Comprehension is severely impaired across modalities, with difficulty understanding spoken
or written language.
D. Conduction Aphasia:
Fluency: Generally fluent speech with occasional word-finding difficulties and phonemic paraphasias (sound
substitutions).
Repetition: Repetition is specifically impaired, with difficulty repeating words or phrases accurately.
Comprehension: Comprehension is relatively preserved, although there may be difficulty with complex or
ambiguous sentences.
E. Anomic Aphasia:
Fluency: Generally fluent speech, but with frequent word-finding difficulties, pauses, and circumlocutions
(describing words instead of naming them directly).
Repetition: Repetition is typically intact or relatively preserved.
Comprehension: Comprehension is generally preserved, although word-finding difficulties may impact
comprehension indirectly.
F. Transcortical Motor Aphasia:
Fluency: Non-fluent speech similar to Broca's aphasia, characterized by effortful and halting production.
Repetition: Repetition is typically preserved, with the ability to repeat words or phrases despite impaired
spontaneous speech.
Comprehension: Comprehension is relatively preserved, although there may be difficulty with complex
syntactic structures.
G. Transcortical Sensory Aphasia:
Fluency: Fluent speech similar to Wernicke's aphasia, but with semantic paraphasias (substituting words with
similar meanings) and neologisms.
Repetition: Repetition is typically intact or relatively preserved.
Comprehension: Comprehension is significantly impaired, resembling Wernicke's aphasia, with difficulty
understanding spoken or written language.
9.3 most common locations of spontaneous ruptured aneurysms in the brain?
Anterior Communicating Artery (ACoA): The junction between the two anterior cerebral arteries.
Middle Cerebral Artery (MCA): The main artery supplying blood to the lateral aspects of the brain.
Internal Carotid Artery (ICA) bifurcation: The point where the ICA divides into the MCA and the anterior
cerebral artery.
10. 5 most common site of hypertensive hemorrhage
Basal Ganglia: This includes the putamen, globus pallidus, and caudate nucleus. Basal ganglia hemorrhages
are the most common type of hypertensive hemorrhage.
Thalamus: Hemorrhage in the thalamus can result in significant neurological deficits.
Pons: Hemorrhages in the pons can lead to profound neurological impairment.
Cerebellum: Hemorrhage in the cerebellum can cause ataxia, headache, and signs of increased intracranial
pressure.
Subcortical white matter: Hemorrhages can occur in the white matter regions surrounding the ventricles.
11. Px with stroke, how do you define the following
12. In PE, why is it important to determine handedness
13. Age “stroke in the young”
Collateral Circulation: The Circle of Willis serves as a vital collateral circulation system. It is formed by the
merging of several major arteries at the base of the brain, including the two internal carotid arteries
(supplying the anterior circulation) and the two vertebral arteries (supplying the posterior circulation). This
interconnected network allows for alternative routes for blood flow if there is an occlusion or stenosis in
 one of the major arteries supplying the brain. In such situations, blood can be rerouted through the Circle
of Willis to ensure continuous perfusion to critical brain regions, reducing the risk of ischemic damage.

Compensation for Variations: The Circle of Willis exhibits natural anatomical variations in its structure and
completeness among individuals. Understanding these variations is important because it determines the
effectiveness of collateral circulation. For example, if one major artery is compromised, the presence of a
well-developed Circle of Willis with adequate connections can compensate for the reduced blood flow by
redirecting it through alternative pathways.

Ischemic Stroke Protection: The Circle of Willis plays a crucial role in protecting the brain against ischemic
strokes, which occur due to blockage or reduced blood flow to a particular region of the brain. In cases
where a major artery supplying the brain becomes occluded (e.g., due to an embolus or atherosclerosis),
the Circle of Willis can provide a backup supply of blood. This collateral flow helps maintain perfusion to
affected brain regions and reduces the risk of tissue damage and neurological deficits associated with
ischemic strokes.

Hemodynamic Stability: The Circle of Willis helps equalize blood flow and pressure between the cerebral
hemispheres and the anterior and posterior regions of the brain. This ensures a balanced supply of blood
and oxygen to different areas, promoting optimal brain function. It helps maintain stable cerebral perfusion
and prevents significant disparities in blood flow that could lead to ischemia or compromised brain function.

Clinical Relevance: Understanding the anatomy and function of the Circle of Willis is crucial for clinical
practice. Knowledge of its variations and potential limitations in collateral circulation aids in interpreting
diagnostic imaging studies, planning surgical interventions, and assessing the risk of ischemic events in
patients with vascular diseases or those undergoing certain procedures.

14. Age “Early onset dementia”

15. 3 types of Cerebral edema
1. Vasogenic Edema:
Vasogenic edema occurs when there is an increase in the permeability of the blood-brain barrier (BBB),
allowing fluid and plasma proteins to leak into the brain tissue.
Causes: Vasogenic edema can result from various conditions such as brain tumors, brain abscesses, brain
trauma, ischemic stroke, or inflammation due to autoimmune disorders (e.g., multiple sclerosis).
2. Cytotoxic Edema:
Cytotoxic edema occurs due to the swelling of brain cells themselves, primarily neurons and glial cells.
Causes: It is often caused by cellular dysfunction or injury, such as cerebral ischemia (lack of blood flow),
metabolic disturbances (e.g., hyponatremia, hypoglycemia), or toxic substances (e.g., carbon monoxide
poisoning).
3. Interstitial Edema (Hydrocephalic Edema):
Interstitial edema involves the accumulation of fluid within the brain's ventricular system and surrounding
spaces.
Causes: It is typically associated with disturbances in the production, circulation, or absorption of cerebrospinal
fluid (CSF). This can occur in conditions such as hydrocephalus (excessive CSF accumulation),
obstructive hydrocephalus (blockage of CSF flow), or conditions affecting the CSF pathways (e.g., tumors,
inflammation).

16. Patient with a history of worst headache of my life/thunderclap headache and vomiting. What is
your impression?
SAH is often characterized by a sudden and severe headache that reaches maximum intensity within seconds
to minutes. It is often described as the worst headache ever experienced by the patient. Vomiting is a
common accompanying symptom. Other possible associated symptoms may include neck stiffness,
photophobia (sensitivity to light), and altered mental status.
17. Enumerate at least 5 signs/ symptoms of increased intracranial pressure?
Headache:
Headache is a common symptom associated with increased ICP. The headache is often described as
persistent, severe, and progressively worsening.
The mechanism behind the headache is thought to be related to the stretching or compression of
pain-sensitive structures within the brain and meninges.
Patients may report that the headache worsens in the morning or upon awakening and may be associated with
nausea or vomiting.

Altered Mental Status:

Increased ICP can affect brain function, leading to changes in mental status. Patients may present with
confusion, irritability, drowsiness, or decreased level of consciousness.
The underlying mechanisms of altered mental status in increased ICP involve compression or displacement of
brain tissue, impaired cerebral perfusion, and disruption of normal neurotransmitter activity.

Vision Changes:
Increased ICP can impact the optic nerve and visual pathways, leading to visual disturbances.
Patients may complain of blurred vision, double vision (diplopia), or even complete loss of vision in severe
cases. These visual changes occur due to the compression of optic structures within the brain, resulting in
impaired transmission of visual signals.

Nausea and Vomiting:

Nausea and vomiting are frequent symptoms associated with increased ICP.
The exact mechanism behind these symptoms is not fully understood, but it is believed to involve stimulation of
the vomiting centers in the brainstem due to increased pressure on surrounding structures.
Patients may experience episodes of nausea and vomiting, particularly in the morning or with changes in body
position.

Seizures:
Increased ICP can irritate brain tissue and disrupt normal electrical activity, leading to seizures.
Seizures associated with increased ICP can manifest as generalized tonic-clonic seizures (convulsions) or
focal seizures, depending on the specific regions of the brain affected.
The underlying mechanisms of seizures in increased ICP involve the distortion of neuronal membranes and
the alteration of ion concentrations.

18. What maneuvers do you do to reduce intracranial pressure?

1. Head Elevation: Elevating the head of the bed to 30 degrees or higher helps promote venous drainage from
the brain, thus reducing intracranial pressure.

2. Cerebrospinal Fluid Drainage: In cases where elevated ICP is caused by increased cerebrospinal fluid
(CSF) volume or impaired CSF absorption, drainage may be necessary. This can be achieved through the
placement of an external ventricular drain (EVD) or lumbar drain to remove excess CSF and lower
intracranial pressure.
3. Sedation and Analgesia: Administering sedatives and analgesics helps reduce agitation, pain, and stress,
which can contribute to increased ICP. Medications such as propofol or dexmedetomidine are commonly
used for this purpose.

4. Hyperventilation: Controlled hyperventilation involves adjusting the respiratory rate and tidal volume to lower
the partial pressure of carbon dioxide (PaCO2) through mechanical ventilation. This causes
vasoconstriction in the brain, reducing cerebral blood volume and intracranial pressure. However,
hyperventilation should be carefully managed to avoid excessively low PaCO2 levels, which can
compromise cerebral perfusion.

5. Osmotic Therapy: Administering osmotic agents such as mannitol or hypertonic saline can help reduce
cerebral edema. These agents create an osmotic gradient, drawing fluid out of brain tissue and into the
bloodstream, thereby reducing intracranial pressure.

6. Barbiturate Coma: In refractory cases of elevated ICP, induction of a barbiturate coma may be considered.
Medications like thiopental or pentobarbital are administered to reduce cerebral metabolic demand and
lower intracranial pressure. This approach is typically used in critical care settings under close monitoring.

7. Decompressive Craniectomy: In severe and uncontrolled cases of elevated ICP, a decompressive

craniectomy may be performed. This surgical procedure involves removing a portion of the skull to provide
more space for the swollen brain, relieving intracranial pressure.

19.

28. Generalized symmetric spike and slow wave discharges that begin and end suddenly. Type of
seizure?
The description you provided, specifically "generalized symmetric spike and slow wave discharges that begin
and end suddenly," is characteristic of a seizure pattern known as "Generalized Tonic-Clonic Seizure" or
"Grand Mal Seizure."

Generalized Tonic-Clonic Seizures involve widespread electrical activity throughout the brain, resulting in loss
of consciousness and a combination of tonic (muscle stiffening) and clonic (rhythmic jerking) phases. The
sudden onset and termination of the seizure activity, along with the presence of generalized spike and slow
wave discharges, are consistent with this seizure type.

1. Generalized Tonic-Clonic Seizures:

- Generalized spike and slow wave discharges.
- High-amplitude, generalized, synchronous epileptiform activity during the tonic and clonic phases.

2. Absence Seizures:
- Generalized 3 Hz spike and slow wave discharges.
- Bilateral and symmetric spike and wave complexes.
- Abrupt onset and termination of the discharges.

3. Focal (Partial) Seizures:

- Focal epileptiform activity originating from a specific region of the brain.
- Sharp waves, spikes, or spike-and-wave complexes in a localized area.
- The location and morphology of the discharges depend on the specific brain region involved.
4. Complex Partial Seizures:
- Focal epileptiform activity often originating from the temporal lobe.
- The presence of rhythmic temporal theta activity or sharp waves in the affected hemisphere.
- Slow wave activity and/or attenuation of background activity during the ictal period.

5. Simple Partial Seizures:

- Focal epileptiform activity restricted to a specific region of the brain.
- Sharp waves, spikes, or slow waves in a localized area without generalization.
- The specific EEG pattern depends on the brain region involved.

29. Myoclonic movements but awake

30. Most common seizure type in metabolic derangements?

The most common seizure type observed in metabolic derangements is "Generalized Tonic-Clonic Seizures"
(previously known as "Grand Mal Seizures"). These seizures are often associated with metabolic
imbalances affecting the entire brain rather than specific focal regions.

Metabolic derangements can disrupt the normal balance of chemicals and electrolytes in the body, leading to
abnormal electrical activity in the brain. Some of the common metabolic disturbances that can trigger
seizures include:

1. Hypoglycemia (low blood sugar): Inadequate glucose supply to the brain can impair its energy metabolism,
leading to abnormal electrical discharges and subsequent seizures.

2. Hyperglycemia (high blood sugar): Severely high blood glucose levels, especially in the setting of diabetic
ketoacidosis, can cause electrolyte imbalances and alterations in brain function, potentially leading to
seizures.

3. Hyponatremia (low sodium levels): Significant decreases in sodium levels disrupt the normal functioning of
nerve cells, including those in the brain, increasing the likelihood of seizures.

4. Hypernatremia (high sodium levels): Markedly elevated sodium levels can result in cellular dehydration and
hyperexcitability, increasing the risk of seizures.

5. Hypocalcemia (low calcium levels): Calcium plays a vital role in neuronal excitability and signaling. A
decrease in calcium levels can lead to hyperexcitability of neurons, potentially manifesting as seizures.

6. Hypercalcemia (high calcium levels): Excessive calcium levels can also cause abnormal neuronal
excitability, potentially leading to seizures.

7. Hepatic encephalopathy: Liver dysfunction can lead to elevated levels of ammonia and other toxins,
resulting in metabolic disturbances and seizures.

Infants and Young Children:

Febrile Seizures: Seizures that occur in association with a fever, commonly between the ages of 6 months and
5 years. They are usually brief and self-limiting.
Benign Rolandic Epilepsy (also known as benign epilepsy with centrotemporal spikes): Characterized by
seizures affecting the face, mouth, and sometimes hand on one side of the body during sleep or upon
awakening.
Children and Adolescents:
Absence Seizures: Brief episodes of impaired consciousness, often characterized by staring spells, temporary
loss of awareness, and subtle movements such as eye blinking or lip smacking.
Juvenile Myoclonic Epilepsy: Primarily characterized by myoclonic jerks (brief muscle twitches) upon
awakening, generalized tonic-clonic seizures, and sometimes absence seizures.

Adults:
Focal (Partial) Seizures: Seizures that originate in a specific area of the brain. They can present with various
symptoms depending on the brain region involved, such as focal motor activity, sensory changes, or
alterations in consciousness.
Generalized Tonic-Clonic Seizures: Seizures characterized by loss of consciousness, muscle stiffening (tonic
phase), and subsequent rhythmic jerking (clonic phase) of the extremities.

Older Adults:
Focal (Partial) Seizures: Similar to adults, older adults may experience focal seizures originating from a
specific area of the brain. However, seizures in this population are often associated with underlying
structural brain abnormalities, such as stroke or brain tumors.
Non-Epileptic Seizures: Seizure-like episodes that are not caused by abnormal electrical discharges in the
brain but rather by underlying medical or psychological factors.

31. Can a patient be diagnosed with a focal and generalized seizure?

32. Sudden jerking motion on R leg when trying to sleep. Chief complaint?

40. 4 phases of migraine headache

Prodrome Phase:

The prodrome phase occurs hours to days before the onset of the headache.
Symptoms during this phase can include mood changes, irritability, fatigue, food cravings, increased urination,
neck stiffness, and increased sensitivity to light or sound.
Some people may also experience aura symptoms during the prodrome phase (known as migraine with aura),
such as visual disturbances (flashing lights, blind spots, zigzag lines), sensory changes, or difficulty
speaking.

Aura Phase:
The aura phase occurs in some individuals with migraines and usually lasts up to one hour but can vary.
Auras are temporary neurological symptoms that typically involve visual disturbances but can also affect other
senses, such as touch or speech.
Visual disturbances can include seeing flashes of light, blind spots, zigzag lines, or temporary vision loss.
Other aura symptoms may include tingling sensations, numbness, difficulty speaking, or confusion.

Headache Phase:
The headache phase is the main phase of the migraine attack and can last from a few hours to several days.
It is characterized by a pulsating or throbbing headache, usually on one side of the head, but it can also be
bilateral.
The headache is typically moderate to severe in intensity and is often accompanied by other symptoms such
as nausea, vomiting, sensitivity to light (photophobia), and sensitivity to sound (phonophobia).
Physical activity may worsen the headache, and individuals may prefer to rest in a quiet, darkened room.
Postdrome Phase:
The postdrome phase occurs after the headache resolves and can last several hours to days.
It is often referred to as the migraine hangover phase.
During this phase, individuals may feel exhausted, weak, or fatigued.
Some people may experience a sense of relief after the headache phase, while others may feel lingering
symptoms such as difficulty concentrating, mood changes, or mild headache.

35. Familial disease

Autism Spectrum Disorder (ASD):
Characteristics: Individuals with ASD typically exhibit difficulties in social interaction, communication, and
repetitive or restricted behaviors. They may have challenges in understanding and responding to social
cues, difficulties with verbal and non-verbal communication, and a preference for sameness or repetitive
behaviors. Sensory sensitivities and specific interests may also be present.
Explanation: ASD is believed to have a multifactorial etiology, with genetic and environmental factors
contributing to its development. Alterations in brain connectivity and neurotransmitter imbalances are
thought to play a role in the manifestation of ASD symptoms.

Fragile X Syndrome:
Characteristics: Fragile X syndrome is characterized by intellectual disability, language and speech delays,
social and behavioral challenges, and physical features such as a long face and large ears. Hyperactivity,
anxiety, and autistic-like behaviors may also be observed.
Explanation: Fragile X syndrome is caused by a mutation in the FMR1 gene, which leads to reduced or absent
production of the fragile X mental retardation protein (FMRP). The absence of FMRP disrupts normal
synaptic development and function, contributing to the cognitive and behavioral features of the disorder.

Rett Syndrome:
Characteristics: Rett syndrome primarily affects females and is characterized by a loss of purposeful hand
skills, loss of spoken language, motor abnormalities (such as hand-wringing or repetitive movements),
breathing abnormalities, and severe intellectual disability. Individuals with Rett syndrome may also have
social and behavioral challenges.
Explanation: Rett syndrome is caused by mutations in the MECP2 gene. MECP2 is responsible for regulating
gene expression, and its dysfunction disrupts normal brain development and function. The loss of MECP2
function primarily affects neurons, leading to the characteristic features of Rett syndrome.

Down Syndrome:
Characteristics: Down syndrome, also known as trisomy 21, is characterized by intellectual disability,
developmental delays, distinct facial features (such as upward slanting eyes and a flattened nasal bridge),
and various health issues. Individuals with Down syndrome may also have a higher risk of heart defects,
respiratory problems, and certain medical conditions.
Explanation: Down syndrome is caused by the presence of an extra copy of chromosome 21. The additional
genetic material affects brain development and function, leading to the cognitive and physical
characteristics observed in individuals with Down syndrome.

Angelman Syndrome:
Characteristics: Angelman syndrome is characterized by developmental delays, severe intellectual disability,
speech impairments or lack of speech, motor coordination difficulties, a happy disposition, frequent
laughter, and an affinity for water. Individuals may exhibit hyperactivity, sleep disturbances, and unique
behavioral features.
Explanation: Angelman syndrome results from the loss or dysfunction of the UBE3A gene, typically due to a
deletion or mutation in the chromosome 15 inherited from the mother. UBE3A is important for normal brain
development and function, and its absence or dysfunction disrupts synaptic processes, contributing to the
clinical features of Angelman syndrome.

37. Myasthenia Gravis

Myasthenia gravis is a chronic condition where the body's immune system mistakenly attacks the receptors for
acetylcholine, a chemical messenger responsible for transmitting signals from nerves to muscles. These
receptors are located at neuromuscular junctions, which are the points where nerves connect to muscle
fibers.
The cardinal features of myasthenia gravis are muscle weakness and fatigability. Muscle weakness is the main
symptom and can affect various muscles, but commonly involves the muscles controlling eye movements,
facial expressions, swallowing, and breathing.
One characteristic of myasthenia gravis is fatigability, which means that the muscle weakness worsens with
repeated or sustained use of the affected muscles. For example, a person with myasthenia gravis may find
it challenging to keep their eyes open for an extended period or experience difficulty swallowing after
eating for a while. However, with rest, the muscle strength improves.
Ocular symptoms are frequently observed in myasthenia gravis. Ptosis, which is drooping of the eyelids, can
affect one or both eyelids and tends to worsen throughout the day or with prolonged use of the eyelid
muscles. Diplopia, or double vision, can occur due to weakness in the muscles that control eye
movements, leading to misalignment of the eyes.
In addition to ocular symptoms, myasthenia gravis can cause weakness in muscles involved in chewing,
swallowing, speaking, and facial expressions. This can result in difficulties with activities like chewing food,
swallowing liquids, speaking clearly, and displaying facial expressions.
In severe cases or during myasthenic crises, which are acute exacerbations of symptoms, respiratory muscles
can be affected. This can lead to shortness of breath, difficulty breathing, and potentially respiratory failure,
requiring immediate medical attention.
Treatment for myasthenia gravis aims to improve muscle strength and manage symptoms. Medications that
enhance the action of acetylcholine or suppress the immune system may be used. In some cases, surgical
removal of the thymus gland (thymectomy) can be considered. Regular follow-up and monitoring are
necessary to adjust treatment as needed.