CNS Flashcards
1
Q
What is the function of the Olfactory nerve (CN I)?
A
It serves the sense of smell.
2
Q
What are common causes of lesions affecting the Olfactory nerve (CN I)?
A
Tumors on the floor of the anterior fossa, head injury, and Alzheimer’s disease.
3
Q
What is the effect of lesions in the Olfactory nerve (CN I)?
A
Anosmia (loss of the sense of smell).
4
Q
What is the function of the Optic nerve (CN II)?
A
Vision.
5
Q
What types of conditions can cause lesions in the Optic nerve?
A
Diabetes, ischemic neuropathy, multiple sclerosis, viral infections (measles, mumps), optic nerve glioma, trauma, and toxins like methyl alcohol.
6
Q
What are the effects of Optic nerve lesions?
A
Unilateral visual loss starting as central or paracentral scotoma.
7
Q
Name a visual defect associated with a retinal lesion.
A
Paracentral scotoma.
8
Q
What visual defect results from an optic tract lesion?
A
Homonymous hemianopia.
9
Q
Name a visual defect associated with an optic nerve lesion.
A
Monocular field loss.
10
Q
What is the function of the Oculomotor nerve (CN III)?
A
It innervates all extraocular muscles except the superior oblique and lateral rectus, and supplies parasympathetic fibers to the ciliary ganglion.
11
Q
What are the types of lesions affecting the Oculomotor nerve (CN III)?
A
Diabetes mellitus, posterior communicating artery aneurysm, giant cell arteritis, raised intracranial pressure (ICP), uncal herniation, and syphilis.
12
Q
How can you differentiate ptosis due to CN III palsy from Horner’s syndrome?
A
• CN III palsy: Severe ptosis, pupil dilated (mydriasis), eye down and out
• Horner’s syndrome: Mild ptosis, pupil constricted (miosis), normal eye position.
13
Q
What is a characteristic effect of a complete CN III lesion?
A
Unilateral complete ptosis, eye facing down and out, and a dilated pupil fixed to light and convergence.
14
Q
What is the function of the Trochlear nerve (CN IV)?
A
It innervates the superior oblique muscle, which depresses the eye and moves it laterally.
15
Q
What are common causes of Trochlear nerve lesions?
A
Head injury (trauma to the orbit) or congenital abnormalities.
16
Q
What are the effects of Trochlear nerve lesions?
A
• Torsional diplopia (double vision at an angle) when looking down
• Eye appears up and inward
• Head tilted away from the lesion.
17
Q
What is the function of the Abducent nerve (CN VI)?
A
It innervates the lateral rectus muscle, responsible for lateral eye movement (abduction).
18
Q
What types of lesions affect the Abducent nerve (CN VI)?
A
Diabetes, multiple sclerosis, pontine cerebrovascular accidents (CVA), tumor infiltration, cavernous sinus thrombosis, and high intracranial pressure (if bilateral).
19
Q
What are the effects of Abducent nerve lesions?
A
• Inability to look laterally (abduction beyond midline is lost)
• Medial squint (unopposed pull of medial rectus)
• Horizontal diplopia.
20
Q
What is the function of the Trigeminal nerve (CN V)?
A
It has both sensory and motor functions:
• Sensory: Skin of the face and scalp, cornea, mucosa of oral and nasal cavities, anterior two-thirds of the tongue
• Motor: Muscles of mastication and tensor tympani.
21
Q
What types of lesions affect the Trigeminal nerve?
A
Pathology within the brainstem (infarct, tumor, multiple sclerosis), cerebellopontine angle (acoustic neuroma), middle ear infection, cavernous sinus aneurysms, and skull base pathology.
22
Q
What are the effects of complete Trigeminal nerve lesions?
A
• Unilateral sensory loss on the face, tongue, and buccal mucosa
• Paralysis of muscles of mastication
• Jaw deviation toward the side of the lesion
• Diminished corneal reflex.
23
Q
What condition is associated with paroxysms of severe facial pain in the Trigeminal nerve distribution?
A
Trigeminal neuralgia (Tic douloureux).
24
Q
What is the function of the Facial nerve (CN VII)?
A
• Sensory: Taste from the anterior two-thirds of the tongue (via chorda tympani)
• Motor: Innervates muscles of facial expression, stapedius, stylohyoid, and posterior belly of the digastric
• Parasympathetic: Secretomotor fibers to submandibular, sublingual, nasal, and palatine glands.
25
What types of lesions affect the Facial nerve?
Brainstem lesions (tumors, multiple sclerosis), Bell’s palsy (HSV), Ramsay Hunt syndrome, skull fractures, parotid gland tumors, Guillain-Barré syndrome, and otitis media.
26
What are the effects of a Facial nerve lesion?
• UMN lesion: Paralysis of contralateral lower face, sparing the forehead
• LMN lesion: Paralysis of the entire ipsilateral face, loss of taste from the anterior two-thirds of the tongue, hyperacusis.
27
How do you differentiate between UMN and LMN lesions of the Facial nerve?
• UMN lesion: Forehead spared, contralateral lower face paralysis
• LMN lesion: Forehead involved, ipsilateral whole face paralysis.
28
What is the function of the Vestibulocochlear nerve (CN VIII)?
• Vestibular component: Balance and equilibrium
• Cochlear component: Hearing.
29
What types of lesions affect the Vestibulocochlear nerve?
Brainstem pathology, cerebellopontine angle tumors (e.g., acoustic neuroma), trauma, middle ear infections.
30
What are the effects of Vestibulocochlear nerve lesions?
• Vestibular: Vertigo, vomiting, nystagmus, ataxia
• Cochlear: Sensorineural hearing loss, tinnitus.
31
What is the function of the Glossopharyngeal nerve (CN IX)?
• Sensory: Taste from the posterior one-third of the tongue, sensation from pharynx and tonsillar sinus
• Motor: Stylopharyngeus muscle
• Parasympathetic: Secretomotor fibers to the parotid gland.
32
What types of lesions affect the Glossopharyngeal nerve?
Brainstem lesions, deep lacerations of the neck.
33
What are the effects of Glossopharyngeal nerve lesions?
Loss of taste from the posterior one-third of the tongue and loss of sensation on the ipsilateral side of the soft palate.
34
What is the function of the Vagus nerve (CN X)?
• Sensory: General sensations from the pharynx, larynx, tracheobronchial tree, heart, and GI tract
• Motor: Palate, pharynx, larynx, trachea, and gastrointestinal tract
• Parasympathetic: Regulation of heart and GI functions.
35
What are the effects of Vagus nerve lesions?
• Palate weakness
• Uvula deviates away from the side of the lesion.
36
What is the function of the Accessory nerve (CN XI)?
It provides motor innervation to the sternocleidomastoid and trapezius muscles.
37
What types of lesions affect the Accessory nerve?
Laceration injuries to the neck.
38
What are the effects of Accessory nerve lesions?
• Paralysis of the sternocleidomastoid and trapezius muscles
• Shoulder drooping on the ipsilateral side.
39
What is the function of the Hypoglossal nerve (CN XII)?
It provides motor innervation to the intrinsic and extrinsic muscles of the tongue (except palatoglossus (vagus)).
40
What are the effects of Hypoglossal nerve lesions?
• Ipsilateral tongue weakness
• Tongue deviates toward the side of the lesion upon protrusion.
41
What cranial nerves are involved in the pupillary light reflex?
• Afferent: CN II (Optic)
• Efferent: CN III (Oculomotor).
42
What cranial nerves are involved in the corneal reflex?
• Afferent: CN V (Trigeminal – ophthalmic division)
• Efferent: CN VII (Facial).
43
What is the difference between bulbar and pseudobulbar palsy?
• Bulbar palsy: LMN lesion affecting CN IX to XII
• Pseudobulbar palsy: UMN lesion affecting corticobulbar tract.
44
What are symptoms of bulbar palsy?
Dysarthria, dysphagia, nasal regurgitation, tongue atrophy, weak gag reflex.
45
What are symptoms of pseudobulbar palsy?
Dysarthria, dysphagia, spastic tongue with no fasciculations, exaggerated gag and jaw reflex.
46
What are the key signs of Midbrain syndromes?
Cranial nerve III and IV involvement: diplopia, ptosis, dilated pupils
47
What are the key signs of Pontine syndromes?
Cranial nerve VI and VII involvement: facial weakness, diplopia
## Footnote
Loss of eye abduction
48
What are the key signs of Medullary syndromes?
Cranial nerves IX, X, XII involvement
Dysarthria, dysphagia, tongue and uvula deviation
49
What tracts are affected in medial brainstem syndromes?
Corticospinal tract: Motor weakness or hemiplegia
Medial lemniscus: Loss of vibration and position sense
50
What tracts are affected in lateral brainstem syndromes?
Spinothalamic tract: Loss of pain and temperature sensation
Sympathetic tract: Horner's syndrome (ptosis, miosis, anhidrosis)
Spinocerebellar tract: Ataxia and cerebellar signs
51
Which side do cranial nerve lesions typically affect in brainstem syndromes?
Cranial nerve lesions are ipsilateral except for palate/uvula deviation (contralateral).
52
Which side do tract lesions typically affect in brainstem syndromes?
Tract lesions are usually contralateral except for sympathetic (ipsilateral) and spinocerebellar (ipsilateral) lesions.
53
What artery is involved in Medial Midbrain Syndrome?
Paramedian branches of the basilar artery.
54
What are key features of Medial Midbrain Syndrome?
Contralateral motor impairment
Ipsilateral CN III palsy (eye down and out, dilated pupil, ptosis)
55
What artery is involved in Medial Pontine Syndrome?
Paramedian branches of the basilar artery.
56
What are key features of Medial Pontine Syndrome?
Contralateral motor weakness
Contralateral vibration and proprioception impairment
Ipsilateral CN VI palsy (inability to abduct the eye)
57
What artery is involved in Lateral Pontine Syndrome?
Anterior inferior cerebellar artery (AICA).
58
What are key features of Lateral Pontine Syndrome?
Ipsilateral ataxia
Ipsilateral facial numbness and palsy (CN V and VII)
Contralateral loss of pain and temperature sensation
59
What artery is involved in Medial Medullary Syndrome?
Anterior spinal artery.
60
What are key features of Medial Medullary Syndrome?
Contralateral motor impairment
Contralateral loss of vibration and proprioception
Ipsilateral CN XII palsy (tongue deviates toward lesion)
61
What arteries are involved in Lateral Medullary Syndrome?
Posterior inferior cerebellar artery (PICA) or vertebral artery.
62
What are key features of Lateral Medullary Syndrome?
Ipsilateral ataxia
Ipsilateral facial numbness
Ipsilateral Horner’s syndrome
Dysphagia, hoarseness, decreased gag reflex
Contralateral loss of pain and temperature sensation
Palate deviation away from the lesion
63
What causes ischemic stroke?
Thromboembolism: thrombosis at atheromatous plaques or embolism from distant plaques or the heart
Hypercoagulable states: antiphospholipid syndrome
Hypoperfusion: watershed infarction
Other causes: aortic dissection, vasculitis, drug abuse
64
What are modifiable and non-modifiable risk factors for ischemic stroke?
Non-modifiable: age, family history, race (African American), gender
Modifiable: hypertension (most important), smoking, alcohol, diabetes, atherosclerosis, hyperlipidemia
65
What are the symptoms of a Middle Cerebral Artery (MCA) stroke?
Face and arm weakness > leg weakness
Contralateral homonymous hemianopia with ipsilateral gaze deviation
Aphasia if dominant hemisphere is involved
66
What are the symptoms of an Anterior Cerebral Artery (ACA) stroke?
Leg weakness > arm weakness
Cognitive/personality changes
Apraxia
67
What are the symptoms of a Posterior Cerebral Artery (PCA) stroke?
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
68
What are the symptoms of an ischemic stroke affecting the posterior circulation (vertebrobasilar)?
Diplopia
Vertigo, dizziness
Ataxia
Dysarthria and dysphagia
69
What are the common complications of ischemic stroke?
Hemorrhagic transformation: Bleeding into the infarcted area
Cerebral edema: Increased intracranial pressure (ICP)
Seizures: Due to infarction-induced brain irritation
70
What are the five clinical types of lacunar infarcts?
Pure motor stroke: Weakness on one side of the body without sensory or cortical signs
Lesion site: posterior limb of the internal capsule
Pure sensory stroke: Numbness without weakness
Lesion site: ventroposterolateral (VPL) nucleus of the thalamus
Ataxic hemiparesis: Ipsilateral weakness and limb ataxia out of proportion to motor deficit
Lesion site: pons
Sensorimotor stroke: Weakness and numbness on the same side of the body without cortical signs
Lesion site: thalamus + posterior limb of internal capsule
Dysarthria-Clumsy Hand Syndrome: Facial weakness, dysarthria, clumsiness of one hand
Lesion site: pons
71
What is the first-line imaging modality for diagnosing ischemic stroke?
Non-contrast CT scan of the brain (to exclude hemorrhage).
72
What imaging findings indicate ischemic stroke on a non-contrast CT scan?
Hypodense area representing infarction (may be normal in the early stages).
73
What blood tests are important for diagnosing ischemic stroke?
CBC (to check for anemia or polycythemia)
Blood glucose
Lipid profile
Coagulation profile
74
What cardiac tests should be conducted to assess stroke risk?
ECG: Look for atrial fibrillation or recent myocardial infarction
Echocardiogram: Detects mural thrombi or valvular disease
Holter monitoring: For paroxysmal atrial fibrillation
Carotid duplex ultrasound: Detects carotid artery stenosis
75
What is the initial step in managing an acute ischemic stroke?
Ensure airway protection, maintain adequate oxygenation, monitor blood pressure, and control blood glucose (<7.8).
76
What is the time window for administering thrombolytic therapy (tPA)?
3 to 4.5 hours from symptom onset.
77
What are the blood pressure targets for patients receiving and not receiving tPA?
With tPA: BP < 185/110 mmHg
Without tPA: BP < 220/110 mmHg
78
What antiplatelet therapy is recommended after stroke if thrombolytics are not given?
Aspirin 300 mg immediately, then 75-150 mg daily.
If already on aspirin add dipyridamole or switch to clopidogrel
79
What are the rules for administering thrombolytics (tPA)?
Inclusion: NIH Stroke Scale score ≥ 4, no hemorrhage on CT or early hypodenaity affecting 1/3 of MCA territory
Exclusion: Recent surgery, bleeding, severe head trauma, previous ICH, BP > 185/110, blood on CT, coagulation problems, head trauma, glucose <2.8 or >22.
80
What medications are recommended for long-term stroke prevention?
Aspirin or clopidogrel
High-dose statins regardless of LDL levels
Antihypertensives for BP control
IV fluids NS (included it here but its not a long term tx)
81
What is the role of endovascular thrombectomy in ischemic stroke?
It is useful up to 8-12 hours after symptom onset for large vessel occlusion in the anterior circulation.
82
How is increased intracranial pressure managed in ischemic stroke?
Elevate the head of the bed, hyperventilation, and administer mannitol.
83
What is a transient ischemic attack (TIA)?
A focal neurological deficit usually lasting less than 1 hour and resolving completely within 24 hours.
84
What causes transient ischemic attacks (TIA) without infarction?
Focal brain, spinal cord, or retinal ischemia (e.g., amaurosis fugax) without infarction (normal imaging).
85
What are common symptoms of TIA?
Visual field cuts, Dysarthria, Double vision, Vertigo, Numbness or weakness, Focal sensory/motor disturbances.
86
What tool is used to predict the risk of stroke following a TIA?
The ABCD2 score.
87
What are the components of the ABCD2 score?
Age ≥ 60: 1 point, BP ≥ 140/90: 1 point, Clinical features: Unilateral weakness: 2 points, Speech disturbance without weakness: 1 point, Duration: ≥ 60 minutes: 2 points, 10-59 minutes: 1 point, Diabetes: 1 point.
88
What investigations are recommended within 24 hours if the ABCD2 score is ≥ 4 or if there are crescendo TIAs (≥ 2/week)?
MRI, ECG + Holter, echocardiography, carotid ultrasound.
89
What findings on carotid ultrasound warrant endarterectomy?
Stenosis > 70% with symptoms requires intervention; Stenosis < 50% or 100% requires no intervention.
90
What is the chronic treatment for TIA?
Aspirin, Statins, Control of modifiable risk factors.
91
What are the characteristics of Broca’s aphasia?
Slow, laborious, non-fluent speech with spared comprehension. Lesion in the left posterior inferior frontal cortex (superior division of left MCA).
92
What are the characteristics of Wernicke’s aphasia?
Fluent but meaningless speech with poor comprehension. Lesion in the posterior superior temporal cortex (inferior division of left MCA).
93
What is global aphasia?
Severe impairment in all aspects of language; involves both Broca and Wernicke areas.
94
What percentage of strokes are intracerebral hemorrhages (ICH)?
10%.
95
What are the most common causes of intracerebral hemorrhage?
Hypertension (deep white matter, basal ganglia, pons, BS, thalamus, cerebellum), hyaline arteriosclerosis/Charcot Bouchard microaneurysms/slit hemorrhages, Cerebral amyloid angiopathy (lobar hemorrhage).
96
What are the risk factors for Intracerebral Hemorrhage (ICH)?
Hypertension (most common), Age (older adults), Smoking, Excessive alcohol use, Drug use (cocaine, amphetamines), Blood disorders (coagulopathies), Anticoagulant medications.
97
How does cerebral amyloid angiopathy contribute to hemorrhage?
It causes lobar hemorrhages related to Alzheimer’s disease and ApoE mutations (E4 risk, E2 protective).
98
What are the key symptoms of intracerebral hemorrhage (ICH)?
Focal motor/sensory deficits, Severe headache, Nausea and vomiting, Loss of consciousness (LOC), Seizures, Features of increased intracranial pressure (papilledema, bradycardia).
99
What causes progressive worsening of symptoms in ICH?
Expansion of the hematoma.
100
What imaging is mandatory for diagnosing intracerebral hemorrhage?
Immediate non-contrast CT.
101
What is the target systolic blood pressure (SBP) in ICH management?
Between 140-160 mmHg.
102
What medications are used to control blood pressure in ICH?
Labetalol, Nicardipine (Calcium channel blocker).
103
How is anticoagulation reversed in patients with ICH on warfarin?
Prothrombin complex concentrate (PCC), Vitamin K.
104
What are the strategies for reducing increased intracranial pressure (ICP) in ICH?
Elevating the head of the bed, Hyperventilation (rapid relief), Mannitol infusion.
105
When is neurosurgical intervention indicated in ICH?
For large hematomas, brainstem compression, or hydrocephalus.
106
What is used for seizure management in intracerebral hemorrhage?
IV anti-epileptic medications.
107
What is the most common cause of subarachnoid hemorrhage (SAH)?
Head injury.
108
What is the most common cause of spontaneous (non-traumatic) subarachnoid hemorrhage?
Rupture of a saccular (berry) aneurysm or Congenital AVM.
109
Where are saccular aneurysms most commonly located?
In the Circle of Willis, particularly at: Anterior communicating artery, Origin of the posterior communicating artery.
110
What are the major risk factors for aneurysm rupture leading to SAH?
Smoking, Hypertension, Family history, Alcohol and drug use (especially cocaine).
111
What is the classic presentation of subarachnoid hemorrhage?
Sudden onset of the worst headache ever ('thunderclap headache'), Neck stiffness (meningeal irritation), Nausea and vomiting, Subhyaloid hemorrhages ± papilledema, Brief loss of consciousness ± seizures.
112
What sign might be seen if there is mass effect from an aneurysm?
Painful third cranial nerve palsy (ptosis, dilated pupil).
113
What initial imaging is recommended for suspected SAH?
Non-contrast CT scan (within 24 hours).
114
What is the next step if the CT is negative but clinical suspicion of SAH remains high?
Perform a lumbar puncture (after 12 hours) to detect: Increased opening pressure, RBCs in CSF, Xanthochromia (bilirubin in CSF).
115
What imaging is used to determine the cause of SAH after diagnosis?
MR angiography or digital subtraction angiography (DSA).
116
What is the first-line treatment for preventing cerebral vasospasm in SAH?
Nimodipine (Calcium Channel Blocker).
117
What is the target systolic blood pressure (SBP) in SAH management?
Maintain SBP < 160 mmHg using IV Labetalol or Nicardipine.
118
How is rebleeding prevented in SAH?
Surgical clipping or endovascular coiling of the aneurysm (best done within 24 hours).
119
How is hyponatremia due to SAH managed?
Large volumes of 0.9% normal saline to address SIADH and urinary salt loss.
120
What is the secondary prevention for SAH?
Control HTN & stop smoking.
121
What are the major complications of SAH?
Rebleeding (30%), Vasospasm and delayed cerebral ischemia, Increased intracranial pressure (ICP) or hydrocephalus, Hyponatremia (due to SIADH), Seizures, Death.
122
What is the prognosis indicator with the highest significance in SAH?
Glasgow Coma Scale (GCS) > 12 on admission. Age, amount of blood visible on CT.
123
What is a subdural hematoma?
Bleeding between the dura mater and arachnoid membrane due to tearing of bridging veins.
124
What is the primary cause of subdural hematoma?
Head trauma leading to venous bleeding with slow accumulation.
125
What populations are at higher risk for subdural hematoma?
Elderly: Due to brain atrophy, Alcoholics: Increased risk of falls and brain atrophy.
126
What are other risk factors for subdural hematoma?
Previous head injury, Use of anticoagulants and antithrombotic medications.
127
How does subdural hematoma typically present?
Headache, Drowsiness and confusion, Mental status changes, Focal neurological signs (hemiparesis), May progress to coma.
128
What imaging finding is characteristic of subdural hematoma on CT?
Crescent-shaped (concave) hematoma that crosses suture lines.
129
How is subdural hematoma treated?
Symptomatic hematomas: Neurosurgical evacuation; Mild cases: May regress spontaneously.
130
What is an epidural hematoma?
Bleeding between the dura mater and skull, often due to rupture of the middle meningeal artery following temporal bone fracture.
131
What is the characteristic clinical presentation of epidural hematoma?
Immediate loss of consciousness (LOC), Lucid interval (recovery for several hours), Rapid neurological deterioration.
132
What imaging finding is characteristic of epidural hematoma on CT?
Biconvex (lens-shaped) hematoma that does not cross suture lines.
133
What is the definitive treatment for epidural hematoma?
Emergent neurosurgical evacuation.
134
What can occur if epidural hematoma is not treated promptly?
Brain herniation, Midline shift, Death.
135
What is a seizure and What is epilepsy?
A convulsion or transient abnormal event caused by a paroxysmal discharge of cerebral neurons. The continuing tendency to have recurrent seizures.
136
How are seizures classified?
Generalized seizures: Bilateral abnormal electrical activity with bilateral motor manifestations and impaired consciousness. Partial seizures: Electrical activity starts in one area of the brain and may later generalize.
137
What are the types of partial seizures?
Simple partial: Does not affect consciousness or memory. Complex partial: Affects awareness or memory before, during, or immediately after the seizure.
138
What is a generalized tonic-clonic seizure (grand mal)?
Sudden onset of a rigid tonic phase followed by convulsions (clonic phase) with rhythmic muscle jerks and possible tongue biting or urinary incontinence.
139
What follows a generalized tonic-clonic seizure?
A post-ictal phase with flaccid unresponsiveness, confusion, and headache lasting several hours.
140
What is a typical absence seizure (petit mal)?
A brief period where the child ceases activity, stares, and pales for a few seconds, often characterized by 3-Hz spike and wave activity on EEG.
141
What are myoclonic, tonic, akinetic seizures?
Myoclonic is isolated muscle jerking. Tonic is stiffening of the body. Akinetic is cessation of movement, falling, LOC.
142
What is a Jacksonian (motor) seizure?
Jerking movements starting in the corner of the mouth or fingers, spreading to involve limbs on the opposite side, sometimes followed by Todd’s paralysis.
143
What are common features of temporal lobe seizures?
Olfactory and visual hallucinations, feelings of déjà vu or jamais vu, blank staring, hippocampal sclerosis as a primary cause, childhood febrile convulsions are the main RF, a common cause of refractory epilepsy, responsive to surgical resection of the damaged temporal lobe.
144
What are common causes of epilepsy?
Cerebrovascular disease, cerebral tumors, alcohol-related seizures, post-traumatic epilepsy, metabolic disorders (hypoglycemia, hypoxia, hypocalcemia, hyponatremia).
145
What are common seizure triggers?
Flashing lights, abrupt cessation of antiepileptic drugs, alcohol abuse, intercurrent illness, evaluation.
146
What investigations help confirm epilepsy?
Eyewitness account of the attack, EEG (abnormal cortical spikes), brain imaging (CT, MRI), LP & blood culture.
147
How is serum prolactin used in seizure evaluation?
Elevated serum prolactin levels help differentiate generalized epileptic seizures from psychogenic non-epileptic seizures.
148
What actions should be taken to protect a patient during a seizure?
Remove harmful objects nearby, place the patient in a lateral (recovery) position, do NOT restrain movements or put anything in the patient's mouth.
149
What should be administered if oxygen levels drop during a seizure?
Administer oxygen.
150
What investigations are recommended during or immediately after a seizure?
Blood glucose, CBC, urea & electrolytes, calcium and magnesium, drug screen and anticonvulsant levels.
151
What is the role of thiamine in seizure management?
Administer 250 mg IV thiamine if poor nutrition or alcohol abuse is suspected.
152
When should rectal diazepam or buccal midazolam be given?
If a seizure lasts longer than 3 minutes or if seizures are repeated.
153
What monitoring is necessary during acute seizure management?
Cardiorespiratory monitoring, pulse oximetry.
154
What is the first-line treatment for acute seizures lasting longer than 3 minutes?
Lorazepam 4 mg IV at 2 mg/min (repeat after 10 minutes if no response). Resuscitation available.
155
What is given first line if IV access is unavailable?
Rectal diazepam (10-20 mg) or buccal midazolam (10 mg).
156
What is the second-line treatment if seizures persist?
Phenytoin 15 mg/kg IV at 50 mg/min (requires cardiac monitoring).
157
What is the third-line treatment for refractory seizures?
Phenobarbital 10 mg/kg IV or Valproate IV (25 mg/kg).
158
When is intubation and ventilation required?
For seizures lasting over 90 minutes or in refractory cases requiring anesthesia.
159
When is long-term antiepileptic therapy indicated?
Recurrent seizures, single seizure with high recurrence risk (e.g., abnormal EEG or brain lesion).
160
What are the preferred drugs for generalized tonic-clonic seizures?
Sodium valproate, levetiracetam, lamotrigine, carbamazepine.
161
Which antiepileptics are best for pregnancy?
Levetiracetam (Keppra) and Lamotrigine.
162
When can antiepileptic drugs be gradually withdrawn?
After being seizure-free for at least 2 years.
163
What are the drugs used for petit mal (absence) seizures?
Ethosuximide (first-line), Sodium valproate (alternative).
164
What are the drugs used for partial seizures?
Lamotrigine, Carbamazepine, Levetiracetam (Keppra), Sodium valproate, Phenytoin.
165
What is status epilepticus?
A prolonged seizure lasting more than 5 minutes or recurrent seizures without returning to baseline consciousness.
166
What is the #1 trigger for status epilepticus?
Abrupt cessation of antiepileptic drugs.
167
What are other common triggers for status epilepticus?
Alcohol withdrawal, stroke, hemorrhage, or trauma, infections (e.g., meningitis), metabolic derangements (e.g., hypoglycemia, hypoxia), cryptogenic (unknown causes).
168
What are the types of status epilepticus?
Convulsive: Generalized or partial. Non-convulsive: Behavioral changes with continuous epileptiform discharges. Psychogenic: Atypical movements with no epileptic activity on EEG.
169
How is pre-hospital treatment for status epilepticus managed?
Buccal midazolam (10 mg) or rectal diazepam (20 mg) if seizure > 3 minutes or repeated seizures.
170
What is the initial management of status epilepticus in the hospital?
ABCs: Ensure airway, breathing, and circulation. Administer oxygen. Cardiorespiratory monitoring and pulse oximetry. Secure venous access and collect blood for: CBC, electrolytes, drug levels, calcium, magnesium. Check blood glucose; if < 3.3 mmol/L, give thiamine followed by dextrose.
171
What is the first-line treatment for acute control of status epilepticus?
Benzodiazepines: IV lorazepam (0.1 mg/kg/dose, max 4 mg/dose). If no IV access: Rectal diazepam or buccal midazolam.
172
What are the second-line treatments for status epilepticus?
IV Phenytoin (15 mg/kg at 50 mg/min): Requires ECG monitoring due to risk of dysrhythmia. Fosphenytoin (preferred): Avoids phenytoin-related side effects (e.g., purple glove syndrome). Alternatives: IV Valproate (25 mg/kg) or IV Levetiracetam.
173
What is the third-line treatment for refractory status epilepticus?
IV Phenobarbital (10 mg/kg, not exceeding 100 mg/min). Intubation and anesthesia if seizures persist (> 90 minutes): Thiopental, Propofol, or Ketamine. Continuous EEG monitoring in ICU.
174
What is the most common hyperkinetic disorder characterized by rhythmic oscillations due to synchronous contraction of agonist and antagonist muscles?
Tremor.
175
Which type of tremor is associated with Parkinson’s disease and occurs while the hand is at rest?
Resting tremor.
176
What are the key features of benign essential tremor?
Familial (autosomal dominant), worsens with anxiety, improves with alcohol, and treated with propranolol.
177
What is a kinetic tremor?
A tremor that occurs during voluntary movements, such as writing or pouring water.
178
How does a kinetic tremor differ from other types of tremors?
It is present throughout the duration of a voluntary movement.
179
What is an intentional tremor?
A tremor that increases in intensity as the individual approaches the target during a deliberate action.
180
Which test is used to identify an intentional tremor?
Finger-to-nose test.
181
What neurological condition is indicated by the presence of an intentional tremor?
Cerebellar lesions.
182
What movement disorder is characterized by irregular, random, semi-purposeful movements and is commonly seen in Huntington's disease?
Chorea.
183
What is the genetic cause of Huntington’s disease, and what neurotransmitters are depleted?
Autosomal dominant mutation; depletion of GABA and acetylcholine but sparing dopamine.
184
What is Sydenham’s chorea?
A post-streptococcal movement disorder characterized by irregular, fidgety, and semi-purposeful movements.
185
What disorder involves stereotyped movements or sounds that can be controlled voluntarily for short periods?
Tics.
186
What is dystonia?
Abnormal muscle contractions leading to abnormal postures or movements of a body part.
187
What are the types of primary dystonia based on onset?
Young onset: Generalized primary torsion dystonia due to DYT1 gene mutation. Adult onset: Task-specific dystonia (e.g., writer’s cramp, musician’s dystonia).
188
What is torticollis?
A type of focal dystonia where the neck is rotated to one side due to excessive action of one sternocleidomastoid muscle.
189
What is blepharospasm?
A focal dystonia characterized by difficulty in opening the eyes due to spasm of the orbicularis oculi muscle.
190
What are common causes of secondary dystonia?
Brain injury, drugs (dopamine-depleting agents), post-encephalitic syndromes, heredodegenerative conditions (e.g., Parkinsonian syndromes, Huntington’s disease, Wilson’s disease).
191
What is the most effective treatment for focal dystonia?
Botulinum toxin.
192
What disorder presents as sudden electric jerk-like movements of a body part or the whole body?
Myoclonus.
193
What is dyskinesia?
Unwanted, involuntary movements often caused by prolonged use of neuroleptics, such as tardive dyskinesia.
194
How is tardive dyskinesia typically caused?
By prolonged use of dopamine receptor-blocking drugs (neuroleptics).
195
What is ballismus?
Sudden, vigorous, and forceful movements, usually involving a whole limb.
196
What is the most common cause of ballismus?
Stroke affecting the subthalamic nucleus.
197
What is the primary pathophysiology of Parkinson's disease?
Progressive depletion of dopamine-secreting cells in the substantia nigra, leading to motor symptoms and neuropsychiatric manifestations.
198
What protein accumulation is associated with Parkinson's disease?
Alpha-synuclein bound to ubiquitin, forming Lewy bodies.
199
What are the risk factors for Parkinson's disease?
Older age, male gender, exposure to toxins (e.g., MPTP), genetic factors (Parkin gene, alpha-synuclein, ubiquitin carboxyl-terminal hydrolase L1).
200
What are the main motor symptoms of Parkinson's disease?
Resting tremor (4-7 Hz, 'pill-rolling'), rigidity (lead pipe or cogwheel), akinesia or bradykinesia (difficulty initiating and slowing voluntary movement), postural instability (stooped posture, shuffling gait, poor arm swing).
201
What non-motor symptoms are associated with Parkinson's disease?
Psychiatric: Depression, hallucinations, dementia; sensory: Anosmia (loss of sense of smell); autonomic: Orthostatic hypotension, drooling, constipation; cognitive: Impulsivity and cognitive decline.
202
What is the primary treatment for Parkinson's disease?
Levodopa/Carbidopa.
203
What are the early and late side effects of Levodopa/Carbidopa?
Early: Hallucinations; Late: Involuntary movements, on-off phenomenon.
204
Name other medications used in the management of Parkinson's disease.
Dopamine agonists (Ropinirole, Pramipexole, Bromocriptine), monoamine oxidase B inhibitors (Selegiline, Rasagiline), COMT inhibitors (Entacapone, Tolcapone), anticholinergics (Benztropine, Trihexyphenidyl), Amantadine (early/mild disease).
205
What surgical treatment is available for severe Parkinson's disease?
Deep brain stimulation (DBS).
206
What is the most common cause of death in Parkinson's patients?
Bronchopneumonia.
207
What are secondary causes for hypokinetic movement disorders?
Drug induced (e.g., dopamine receptor blocking drugs), post-encephalitic, Wilson’s disease, trauma (dementia pugilistica in boxers).
208
What is multiple sclerosis (MS)?
A chronic autoimmune demyelinating disease affecting the CNS, characterized by progressive damage to oligodendrocytes and white matter plaques.
209
What are the risk factors for MS?
Genetic: HLA-DR2 association; Environmental: Epstein-Barr virus (EBV), HHV6, low vitamin D, smoking; Age: 20-40 years; Gender: More common in females.
210
What hypersensitivity reactions are involved in MS?
Types IV (T-cell-mediated against MBP) and II (AB-mediated against oligodendrocytes & myelin) hypersensitivity reactions.
211
What are common locations for MS plaques?
Optic nerve, periventricular white matter, brainstem and cerebellar connections, cervical spinal cord (CST & PWC).
212
What are the clinical patterns of MS?
Relapsing-remitting (most common, 85%), secondary progressive, primary progressive (10%), relapsing-progressive.
213
What are the key symptoms of MS?
Sensory: Paresthesia, loss of vibration sensation; Motor: Weakness, spasticity, Babinski sign; Optic nerve: Optic neuritis, central scotoma; Cerebellar: Nystagmus, intention tremor, dysarthria; Brainstem: Diplopia, vertigo, dysphagia, facial weakness; Autonomic: Urge incontinence, sexual dysfunction; Cognitive: Depression, memory loss, dementia.
214
What are Lhermitte's and Uhthoff’s signs in MS?
Lhermitte's sign: Tingling electric shock-like sensation on arms, back, leg upon neck flexion. Uhthoff’s sign: Worsening symptoms in hot weather or after a hot bath.
215
How is MS diagnosed?
MRI: Periventricular lesions; CSF: IgG oligoclonal bands, elevated gamma globulins; Evoked potentials: Prolonged latency; Diagnosis requires dissemination in time and space (McDonald criteria).
216
What is the treatment for acute MS attacks?
High-dose pulse IV methylprednisolone (1 gm/day for 3-5 days).
217
What are disease-modifying agents for MS?
Interferon beta-1a/b: Reduces relapse rate by a third (may cause flu-like symptoms); Glatiramer acetate: Similar to myelin basic protein; Natalizumab: Anti-adhesion monoclonal antibody (risk of JC virus activation); Oral agents: Fingolimod, Dimethyl fumarate, Teriflunomide.
218
What are poor prognostic indicators in MS?
Male gender, motor or cerebellar symptoms, high lesion load on MRI, poor recovery after the first relapse.
219
What is Myasthenia Gravis?
An autoimmune disorder of the neuromuscular junction characterized by antibodies against postsynaptic acetylcholine receptors (type II hypersensitivity).
220
What are the key risk factors for Myasthenia Gravis?
Peaks in the 3rd decade for females and 6th decade for males. More common in women. Associated with thymic hyperplasia (70%), thymoma (10%), and other autoimmune conditions (thyroid disorders, rheumatoid arthritis, pernicious anemia).
221
What are the hallmark clinical manifestations of Myasthenia Gravis?
Descending weakness (ocular, bulbar, proximal limb muscles), fatigue with sustained action, improves with rest, ptosis and diplopia, better with sleep or ice pack, difficulty swallowing, chewing, and nasal speech, diurnal variation (worsens at night), respiratory difficulties, normal reflexes.
222
What bedside tests can indicate Myasthenia Gravis?
Counting to 20: fatigue worsens, upward gaze: ptosis appears, relieved by ice packs, outstretched arms: slow downward drift, normal reflexes.
223
What is the most specific investigation for Myasthenia Gravis?
Anti-AChR antibodies. Also test for anti-MuSK ABs.
224
What is the response in nerve stimulation test for MG patients & why?
Decrement response because muscle strength decreases with repeated stimulation.
225
What investigation is the most sensitive for Myasthenia Gravis?
Single fiber electromyography.
226
What is the Tensilon test used for?
Temporary improvement of symptoms with IV anticholinesterase (Edrophonium).
227
What condition mimics Myasthenia Gravis and improves with repeated muscle stimulation?
Lambert-Eaton Myasthenic Syndrome (associated with small-cell lung cancer). Has AB against presynaptic calcium channels, hyporeflexia.
228
What is the primary treatment for Myasthenia Gravis?
Pyridostigmine (anticholinesterase). Immunosuppressants (steroids & azathioprine) if no response to treatment.
229
When is thymectomy indicated in Myasthenia Gravis?
For thymoma or patients under 50 with anti-AChR antibodies.
230
What is a Myasthenic Crisis, and how is it managed?
Life-threatening condition with profound weakness and respiratory involvement. Triggered by infections, surgery, pregnancy, or drugs (aminoglycosides, beta-blockers). Managed with plasmapheresis or IVIg.
231
What are the differential diagnoses for Myasthenia Gravis?
Thyroid ophthalmopathy, myotonic dystrophy, brainstem cranial nerve lesions, motor neuron disease, Lambert-Eaton myasthenic syndrome, botulism (post consumption of contaminated food, clostridium botulinum).
232
What is Guillain-Barré Syndrome (GBS)?
Acute inflammatory demyelinating symmetrical ascending polyneuropathy.
233
What infections commonly precede GBS?
Campylobacter jejuni, Epstein-Barr virus (EBV), and CMV.
234
What are the primary clinical features of GBS?
Ascending symmetrical weakness, loss of reflexes, autonomic dysfunction (postural hypotension, arrhythmias), respiratory failure in severe cases, may include bilateral lower CN 7 palsy & sudden hypotension/tachycardia.
235
What is albumin-cytologic dissociation in GBS?
Elevated CSF protein with normal cell count.
236
What is the first-line treatment for GBS?
IVIg or plasmapheresis. No role for steroids. Heparin for thrombosis.
237
How is respiratory function monitored in GBS?
Pulmonary function tests every 4 hours; ICU transfer if FVC falls below 80% of predicted.
238
What are the major causes of death in Guillain-Barré Syndrome?
Respiratory failure, pulmonary embolism, or infection.
239
What is CIDP and how does it differ from Guillain-Barré Syndrome (GBS)?
CIDP is a chronic, relapsing or progressive inflammatory demyelinating polyneuropathy, whereas GBS is an acute, monophasic illness. CIDP presents with slowly progressive weakness, areflexia, and loss of vibration sense.
240
How is CIDP treated?
First-line treatment is corticosteroids (prednisone). IV immunoglobulin (IVIg) and plasma exchange are alternative options. Long-term treatment with immunosuppressants may be required.
241
What is meningitis?
Inflammation of the meninges, often due to infection.
242
What is the classic triad of acute bacterial meningitis?
Fever, nuchal rigidity, altered mental status.
243
What signs are associated with meningitis?
Kernig’s sign: Pain with knee extension when hip is flexed. Brudzinski’s sign: Neck flexion causes hip and knee flexion.
244
What are common causes of bacterial meningitis in different age groups?
Infants: Group B strep, E. coli, Listeria.
Children: Streptococcus pneumoniae, Neisseria meningitidis, H. influenzae.
Adults: Streptococcus pneumoniae, Neisseria meningitidis.
Elderly: Same as adults, plus Listeria, aerobic gram-negative bacilli.
Immunocompromised: Cryptococcus neoformans & acanthamoeba.
245
What are the CSF findings in bacterial, TB, and viral meningitis?
Bacterial: Turbid, high WBCs, high PMN, high protein, low glucose.
TB: Clear, high WBCs, high lymphocytes, very high protein, low glucose.
Viral: Clear, moderate WBCs, high lymphocytes, high protein, normal glucose.
246
What is the first step in suspected meningitis management?
Stabilize ABCs, draw blood cultures, and perform a lumbar puncture immediately (unless contraindicated, in which case start antibiotics first).
247
What empirical antibiotics are used for meningitis?
General: Vancomycin + 3rd generation cephalosporin. Elderly or immunocompromised: Add ampicillin for Listeria coverage. Empirical for infants: ampicillin + gentamicin.
248
What are the prophylaxis for close contacts?
Rifampin or ciprofloxacin with meningococcal meningitis. Meningococcal septicemia: 3rd generation cephalosporin (cefotaxime) + dexamethasone.
249
What are the indications for a CT scan before lumbar puncture in meningitis?
Papilledema, new-onset seizures, abnormal consciousness, CNS disease history, focal neurological signs, or immunocompromised status.
250
What is the role of dexamethasone in bacterial meningitis?
Reduces neurological complications like deafness, given before or with the first antibiotic dose. Continued with Streptococcus pneumoniae meningitis.
251
How is TB meningitis treated?
Intensive phase (2m): Isoniazid + Rifampin + Pyrazinamide + Moxifloxacin or Streptomycin or levofloxacin. Continuation phase (7m): Isoniazid + Rifampin. Adjunctive corticosteroids (Dexamethasone/Prednisone): Given for 2 weeks high dose, then tapered over 6 weeks.
252
What are the main complications of meningitis?
Neurological: Increased intracranial pressure, cerebral edema, hearing loss, seizures, stroke, hydrocephalus. Systemic: Septic shock, disseminated intravascular coagulation (DIC), multi-organ failure.
253
What is encephalitis?
Inflammation of the brain parenchyma, primarily affecting cerebral function.
254
What are the most common causes of encephalitis?
Viral (most common): Herpes simplex virus (HSV), arbovirus, cytomegalovirus (CMV), varicella-zoster virus (VZV), enteroviruses. Non-viral: Cryptococcus neoformans, Listeria, tuberculosis (TB), autoimmune conditions.
255
What are the key symptoms of encephalitis?
Fever and meningismus (neck stiffness, photophobia), altered level of consciousness (confusion, personality changes, coma), seizures, focal neurological deficits, headache, nausea, vomiting.
256
What diagnostic findings are seen in encephalitis?
MRI/CT scan: Temporal lobe abnormalities in HSV encephalitis, brain swelling, increased ICP, midline shift.
EEG: Periodic sharp and slow wave complexes in HSV encephalitis.
CSF: WBCs: Lymphocytosis (50-500). Protein: Elevated. Glucose: Normal or slightly low. PCR for HSV, CMV, VZV: Confirms viral cause.
257
What is the treatment for viral encephalitis?
HSV encephalitis: Immediate IV acyclovir (10 mg/kg for 14-21 days). Empirical treatment for meningoencephalitis: IV acyclovir + ceftriaxone + vancomycin.
258
What is a brain abscess?
A focal, suppurative infection in the brain parenchyma, often caused by polymicrobial infections, leading to pus collection surrounded by a capsule.
259
What are the common causes of brain abscess?
Sinusitis, chronic otitis media, post-neurosurgery.
Can develop from hematogenous spread (IE, lung abscess, bronchiectasis).
260
What are the most common organisms causing brain abscesses?
Polymicrobial infections: Streptococcus, Staphylococcus aureus, anaerobes.
261
What are the key symptoms of a brain abscess?
Headache (most common symptom), fever, nausea, vomiting, focal neurological deficits (depending on location), seizures, increased intracranial pressure (ICP) → papilledema, CN III and CN VI palsies.
262
What imaging is used to diagnose a brain abscess?
CT scan with contrast: Ring-enhancing lesion with a low-density core (most common finding).
MRI: More sensitive for early cerebritis and edema.
Blood cultures: Identify the causative organism in hematogenous spread.
Lumbar puncture: NOT recommended (risk of brainstem herniation).
263
What is the treatment for a brain abscess?
Broad spectrum IV antibiotics and surgical drainage.
264
What are the pain sources of headaches?
Arteries, veins, meninges, scalp, and muscles, with pain signals transmitted via cranial nerves V and IX and upper cervical nerve roots.
265
What is the mnemonic for headache evaluation?
TOSS IT: Timing, Other symptoms (nausea, photophobia, phonophobia, tearing, ptosis), Site, Severity, Influences (aggravating and relieving factors), Type (character).
266
What are the red flags and secondary causes of headache ?
SNOPP: Systemic symptoms (fever, weight loss),
Neurological signs (confusion, focal deficits),
Onset (sudden thunderclap headache → suspect SAH),
Previous headache history (new pattern, progression),
Postural aggravation (worse with Valsalva, pregnancy → suspect CSF leak or venous thrombosis).
267
How are headaches classified?
Primary Headaches (No underlying cause): Long duration (>4 hours): Tension-type headache, migraine. Short duration (<4 hours): Cluster headaches, paroxysmal hemicrania, SUNCT. Chronic headaches: Chronic tension-type headache, chronic migraine, hemicrania continua, medication-overuse headache.
Secondary Headaches (Identifiable cause): Causes: Brain tumors, meningitis, vascular disorders, systemic infections, head injury, drug-induced.
268
What is the most common primary headache?
Tension-type headache (TTH).
269
What are the key features of a tension-type headache?
Mild to moderate bilateral band-like tightening, non-throbbing pain. No nausea/vomiting. May have muscle tenderness in head and neck.
270
What are common triggers for tension-type headaches?
Stress, sleep deprivation, dehydration, hunger, refractive errors, cervical spondylosis, hypertension.
271
How is a tension-type headache treated?
Acute: NSAIDs (ibuprofen, naproxen, aspirin) or acetaminophen. Prophylaxis (for frequent/chronic cases): Amitriptyline (TCA), stress management.
272
What are the key features of migraine?
Duration: 4-72 hours. Location: Usually unilateral, throbbing, moderate to severe pain. Associated symptoms: Nausea, vomiting, photophobia, phonophobia. Exacerbating factors: Movement, light, noise (patients prefer a dark, quiet room). Relieved by: Sleep.
273
What are migraine triggers?
Lifestyle: Sleep deprivation, stress, weather changes. Dietary: Alcohol, cheese, chocolate, skipping meals, nitrates. Environmental: Bright light, loud noise, physical activity, head injury. Hormonal: Menstruation, menopause, oral contraceptives.
274
What are the complications of migraines?
Prolonged symptoms (>72 hours). Stroke. Seizures. Chronic migraine (≥15 days/month for 3 consecutive months).
275
What are the four phases of a migraine?
Prodrome (mins-48 hours before headache): can have eciyory symptoms or inhibitory symptoms.
Aura (15-60 minutes): Cortical spreading depression causing visual symptoms (scotoma, tunnel vision), sensory symptoms (tingling), or language issues.
Headache (4-72 hours): Vasodilation leading to throbbing pain in the orbitotemporal region.
Postdrome (up to 24 hours): Fatigue, hyperesthesia, difficulty concentrating.
276
How is an acute migraine attack treated?
Mild-moderate: NSAIDs (aspirin, ibuprofen, naproxen, diclofenac) or acetaminophen. Moderate-severe: Triptans (sumatriptan) or triptan + naproxen combination. Emergency migraine treatment: Subcutaneous sumatriptan. IV metoclopramide + diphenhydramine. OR IV dihydroergotamine + metoclopramide.
277
What are contraindications for triptans?
Cardiovascular disease (risk of vasospasm → stroke, CAD).
278
What is the risk of frequent migraine medication use?
Medication-overuse headache.
279
When should migraine prophylaxis be considered?
4-5 attacks/month or long-lasting migraines. Significant disability or reduced quality of life. Risk of neurological damage (hemiplegic migraine, prolonged aura, stroke). Overuse/contraindications to acute treatments.
280
What are the first-line preventive treatments for migraines?
Propranolol: Avoid in diabetics and asthmatics. Valproic acid: Best for men (causes weight gain, PCOS in women). Topiramate: Good for obese women (causes weight loss, kidney stones).
281
What are alternative migraine prevention options?
Riboflavin (Vitamin B2): Safe, 1000 mcg. Magnesium supplementation. Botox injections (31 sites on the scalp & neck every 3 months).
282
What is Trigeminal Autonomic Cephalalgia (TAC)?
A group of strictly unilateral severe headaches with prominent ipsilateral autonomic symptoms affecting the trigeminal nerve.
283
What are the key autonomic symptoms in TAC?
Conjunctival injection & tearing, nasal congestion & rhinorrhea, eyelid edema, forehead & facial sweating, Horner’s syndrome (ptosis, miosis, anhidrosis).
284
What is SUNCT?
Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing. Duration: 5-40 seconds. More common in men (35-65 y/o). Stabbing/electric pain (single, grouped, or sawtooth pattern).
## Footnote
Acute Treatment: IV lidocaine. Prevention: Lamotrigine, topiramate, gabapentin. Does NOT respond to O2 or indomethacin.
285
What is Paroxysmal Hemicrania?
Duration: 15-30 minutes. More common in females. Mean 11-14 attacks per day. Icepack-like pain, recurrent, associated with tearing & rhinorrhea.
## Footnote
Treatment: Indomethacin (complete resolution in 1-2 days). Alternatives: verapamil, aspirin or other NSAIDs (naproxen or diclofenac).
286
What is Cluster Headache?
Duration: 15-180 minutes. More common in males, especially smokers. Pathophysiology: Hypothalamic activation → trigeminal-autonomic reflex. 'Suicide headache' → severe unilateral orbital/supraorbital pain with autonomic symptoms. Circadian rhythmicity: Attacks occur at the same time each day and each year. Trigger: Alcohol. Patients prefer to move during attacks.
287
How are cluster headaches treated?
Abortive treatment: 100% oxygen (10 L/min for 20 min, sitting position). Subcutaneous or nasal triptans. If refractory: Intranasal lidocaine, oral ergotamine, IV dihydroergotamine. Transitional prophylaxis (rapid attack suppression): Prednisone (18 days, mainstay treatment). Greater occipital nerve block. Long-term prophylaxis: Verapamil (CCB). Surgical options: Thermo-ablation of trigeminal ganglion. Deep brain stimulation.
288
What is trigeminal neuralgia (tic douloureux)?
Severe unilateral knife-like or electric shock pain affecting one or more branches of the trigeminal nerve (CN V). Abrupt onset & termination. Triggered by: Washing, eating, shaving.
289
How is trigeminal neuralgia treated?
First-line: Carbamazepine (alternatives: gabapentin, lamotrigine, baclofen). If refractory: Thermocoagulation of the trigeminal ganglion or surgical sectioning of sensory divisions.
290
What is Pseudotumor Cerebri?
A condition of chronically elevated intracranial pressure (ICP) without a clear cause. Idiopathic.
291
What are the symptoms of IIH?
Headache (throbbing), papilledema (bilateral and symmetric), pulsatile tinnitus, transient visual obscurations, enlarged blind spot, CN VI palsy (abducens nerve, unilateral or bilateral).
292
What are the risk factors for IIH?
Obese women of childbearing age, vitamin A intoxication (retinoids), endocrine disorders: Hypothyroidism, hypoparathyroidism, Addison’s, PCOS, SLE, drugs: Growth hormone, tetracyclines, clindamycin, steroid withdrawal.
293
How is IIH diagnosed?
MRI: To exclude other causes of ↑ ICP (empty sella, distended perioptic subarachnoid space, transverse venous sinus stenosis). Lumbar Puncture (LP): Normal CSF composition (protein, glucose, cells).
294
What is the treatment for IIH?
First-line: Weight loss. Medications: Acetazolamide (diuretic), alternative: Topiramate. Severe cases: Optic nerve sheath fenestration. CSF shunting procedure (if progressive vision loss).
295
What is the normal and abnormal range of ICP?
Normal ICP: 8-18 mmHg. Pathologic ICP: Sustained elevation above 20 mmHg.
296
What is the Monro-Kellie Doctrine?
The skull is a fixed volume, so an increase in one compartment (brain tissue, CSF, or blood) must be balanced by a decrease in another to maintain normal ICP. If ICP increase it can cause brain herniation or if it increases above MAP ischemia will occur. Ischemia doesn't occur when CBF is between 60-160 due to autoregulation.
297
What are the symptoms of increased ICP?
Headache (worse with coughing, straining, bending forward, lying flat), morning vomiting (sudden, effortless, without nausea), altered consciousness, speech, sensation, movement disturbances. Visual disturbances: papilledema, transient vision loss (seconds), 'sunsetting sign' in infants (severe hydrocephalus), diplopia.
298
What are the causes of increased ICP?
Generalized brain injury: Toxins, infections, encephalopathies, diffuse head injury, hypoxic-ischemic injury. Focal intracranial injury: Vascular lesions (subdural/epidural hemorrhage, AVM). Focal traumatic lesions: Tumors, abscesses causing CSF obstruction.
299
What are the complications of increased ICP?
Decreased cerebral blood flow → ischemia. Brain herniations: Subfalcine, transtentorial, tonsillar (foramen magnum), central, upward transtentorial herniation.
300
What are the types of brain edema?
Cytotoxic Edema: Intracellular swelling due to ATP failure (e.g., hypoxic-ischemic injury, traumatic brain injury). Tx: Often irreversible, but water intoxication may be reversible.
Vasogenic Edema: Increased capillary permeability, leading to fluid leakage into extracellular space (e.g., tumors, hemorrhage, infections). Tx: Steroids for vasogenic edema due to mass lesions.
Interstitial Edema: Fluid accumulation in white matter due to CSF flow obstruction (e.g., hydrocephalus). Tx: Reducing CSF pressure.
301
What is brain herniation?
The shift of brain tissue through intracranial barriers (tentorial notch, falx cerebri, foramen magnum) due to mass effect and increased pressure.
302
What are the types of brain herniation?
Supratentorial Herniation: Includes uncal, central, subfalcine (cingulate), transcalvarial.
Infratentorial Herniation: Includes tonsillar and upward transtentorial (rarest type).
303
What are the key features of transtentorial herniation?
Uncal Herniation: First sign: Ipsilateral CN III palsy (pupil dilation). Contralateral hemiparesis (cerebral peduncle compression). Occipital lobe infarction (PCA compression).
Central Herniation: Both temporal lobes herniate through the tentorial notch due to bilateral mass effects or diffuse brain edema.
304
What is subfalcine herniation and what are its complications?
The cingulate gyrus displaces under the falx cerebri due to a high supratentorial mass. One or both anterior cerebral arteries (ACA) can be compressed, leading to infarction in the paramedian frontal and parietal lobes. Bridging veins can be compressed, further increasing ICP and causing sudden deterioration.
305
What is tonsillar herniation?
Also called Foramen Magnum Herniation or Coning, where the cerebellar tonsils herniate through the foramen magnum, compressing the medulla oblongata and upper cervical spinal cord, leading to cardiopulmonary irregularities (potentially fatal).
306
What are the general principles of cerebellar disease?
Cerebellar signs are ipsilateral due to double decussation. Cerebellar disease does not cause weakness or involuntary movement but results in errors in movement execution. Medial disease affects the trunk, while lateral disease affects the limbs. Pancerebellar syndrome presents bilaterally and may be due to toxins, metabolic disorders, infections, or autoimmune diseases.
307
What are the clinical signs of cerebellar disease?
Ataxia: Uncoordinated voluntary movements.
Dysmetria: Inability to judge distances, causing overshooting or undershooting (finger-to-nose test).
Dysdiadochokinesia: Impaired ability to perform rapid alternating movements.
Broad-based gait: Clumsy, staggering movements with a wide base.
Nystagmus: Involuntary oscillatory eye movements, especially when looking sideways.
Scanning (slurred) speech (Dysarthria): Poor articulation with long pauses between words.
Intention tremor: Action tremor that worsens as the target is approached.
Hypotonia & vertigo.
308
How do different cerebellar areas affect function?
Cerebellar Hemisphere (Lateral): Causes ipsilateral limb ataxia, dysmetria, dysdiadochokinesia, intention tremor, dysarthria, hypotonia (commonly due to infarct, neoplasm, demyelination).
Flocculonodular Lobe: Affects balance and eye movements, leading to truncal ataxia, vertigo, nystagmus, and abnormal vestibulo-ocular reflex.
Vermis (Midline): Truncal ataxia, gait instability, and limb dysmetria. If rostral vermis is affected, common causes include alcoholism and thiamine deficiency. If caudal vermis is affected, suspect medulloblastoma (children).
309
What are causes of cerebellar dysfunction?
1. Drug-Induced Cerebellar Degeneration (Ataxia): Phenytoin, carbamazepine, phenobarbital, chemotherapy. Symptoms: Wide-based gait, nystagmus, dysmetria, intention tremor.
2. Paraneoplastic Cerebellar Degeneration: Autoantibodies attack Purkinje cells, causing progressive ataxia and abnormal eye movements. Diagnosis: Paraneoplastic antibodies in serum/CSF. Treatment: Tumor removal & immunosuppression.
3. Friedreich’s Ataxia: Autosomal recessive (GAA repeat disorder). Most common hereditary ataxia. Symptoms: Cerebellar signs: Gait/limb ataxia, dysarthria, nystagmus. Neurological signs: Spasticity, Babinski sign, absent reflexes. Muscle wasting, pes cavus (high-arched feet), scoliosis. Cardiac involvement: Hypertrophic cardiomyopathy (50-75%). Diabetes in 10-30%. Death by middle age.
310
What are the sources of brain tumors?
Primary intracranial tumors (10% of neoplasms, rarely metastasize outside CNS). Metastatic tumors (lung, breast, kidney, GI), usually located at the gray-white junction.
311
What are the symptoms of brain tumors?
Progressive focal neurological deficits. Increased ICP (headache, nausea, vomiting, diplopia). Seizures. Psychiatric symptoms, visual field defects.
312
What is an astrocytoma and how does it present?
Types: Diffuse (benign), Anaplastic (malignant), Glioblastoma (highly malignant). Presentation: Headache, seizures, focal neurological deficits. Treatment: Surgical resection, radiation, chemotherapy.
313
What is a glioblastoma and why is it significant?
Most aggressive and malignant type of astrocytoma. Rapid progression and poor prognosis. Highly infiltrative, making complete resection difficult. Treatment: Surgery, radiation, chemotherapy, but prognosis remains poor.
314
What is a meningioma and how does it present?
Benign, slow-growing tumor. More common in women. May be asymptomatic or cause symptoms depending on location. Common symptoms: Cranial nerve dysfunction, seizures, focal neurological deficits. Treatment: Surgical resection; radiation if unresectable.
315
What is a vestibular schwannoma (acoustic neuroma) and how does it present?
Benign tumor of the vestibulocochlear nerve (CN VIII). Symptoms: Unilateral hearing loss, tinnitus, vertigo, balance problems. Treatment: Surgical resection or radiation.
316
What is a pilocytic astrocytoma and how does it present?
Benign, well-circumscribed tumor, usually in the posterior fossa (cerebellum). Common in children. Symptoms: Drowsiness, headache, ataxia, nausea, vomiting, cranial neuropathy. Treatment: Surgical resection, radiation if necessary.
317
What is a medulloblastoma and how does it present?
Highly malignant neuroectodermal tumor, commonly in children. Arises from the 4th ventricle (posterior fossa). Symptoms: Obstructive hydrocephalus, increased ICP, ataxia. Treatment: Surgical resection, radiation, chemotherapy.
318
What is a craniopharyngioma and how does it present?
Most common suprasellar tumor in children. Often contains calcifications. Symptoms: Hypopituitarism, bitemporal hemianopsia (optic chiasm compression). Treatment: Surgical resection.
319
How are brain tumors diagnosed?
CT/MRI with contrast. Histologic biopsy (CT-guided or surgical).
320
How is increased ICP in brain tumors managed?
Head elevation. Hyperventilation (reduces ICP). Corticosteroids, mannitol (reduce cerebral edema).
321
What are the treatment options for brain tumors?
Surgical resection (if possible). Radiation therapy and chemotherapy. Supportive care to manage symptoms and ICP.
322
What is dementia, and what are its key features?
Dementia is a progressive decline in memory and at least one other cognitive function in an alert person. It is irreversible and leads to memory loss, disorientation, impaired judgment, personality changes, and psychosis.
323
What are the risk factors for dementia?
Aging (elderly), female gender, Down’s Syndrome, head injury, systolic hypertension, genetics.
324
What are the reversible causes of dementia?
Hypoglycemia, hypothyroidism, tertiary syphilis, subdural hematoma, vitamin B12 deficiency, normal pressure hydrocephalus.
325
What are the differentials for dementia?
Alzheimer Disease, Vascular Disease, Drugs, Depression, Delirium, Ethanol, Medical/Metabolic Systems, Endocrine, Neurologic, Infection, Idiopathic, Immunologic.
326
How is dementia differentiated from delirium?
Dementia is chronic and irreversible with normal alertness, while delirium is acute and fluctuating with impaired attention and alertness.
327
What is the pathophysiology of Alzheimer’s disease (AD)?
AD is caused by amyloid plaques & neurofibrillary tangles leading to cortical atrophy.
328
What are the clinical stages of Alzheimer’s disease?
Mild AD: Memory loss, confusion, mood changes. Moderate AD: Increased memory loss, language problems. Severe AD: Weight loss, seizures, infections.
329
What is mild cognitive impairment (MCI) in AD?
Intermediate stage between normal aging and AD, characterized by new memory complaints without functional impairment.
330
What are the key features of Lewy Body Dementia?
2nd most common dementia, associated with Parkinson’s, marked cholinergic deficit, fluctuations in cognition, early visual hallucinations.
331
What are the key features of vascular dementia?
3rd most common dementia, caused by multiple strokes/infarcts, presents with stepwise cognitive decline.
332
What are the key features of frontotemporal dementia (Pick’s disease)?
Early personality changes, loss of empathy, socially inappropriate behavior, misdiagnosed as a psychiatric disorder.
333
What are the key features of coma?
Unarousable state with eyes closed, no response to pain, loss of arousal, but brainstem and spinal reflexes may be intact.
334
What are the key features of vegetative state?
Awake but unresponsive, with normal sleep-wake cycles, no meaningful interaction, but preserved reflexes.
335
What is locked-in syndrome?
Conscious but paralyzed, disruption of corticospinal & corticobulbar pathways, with preserved cognition.
336
How is brain death diagnosed?
Irreversible cessation of brain and brainstem function, diagnosed by coma and absent brainstem reflexes.
337
What are the different types of abnormal breathing patterns and their causes?
Cheyne-Stokes respiration, Central neurogenic hyperventilation, Apneustic breathing, Ataxic breathing.
338
What are the clinical features of lower motor neuron (LMN) lesions?
Weakness, muscle atrophy, hyporeflexia, hypotonia, fasciculations, and muscle cramps.
339
What are the causes of LMN lesions?
Poliomyelitis, spinal muscular atrophy, amyotrophic lateral sclerosis.
340
What are the clinical features of an upper motor neuron (UMN) lesion?
No muscle wasting, spasticity, clonus present, brisk deep tendon reflexes, extensor plantar reflex.
341
What are the different types of peripheral neuropathies?
Neuronopathy, Mononeuropathy, Mononeuropathy Multiplex, Polyneuropathy, Radiculopathy.
342
What are the symptoms of Peripheral Nerve Disease?
Negative motor symptoms, Positive motor symptoms, Negative sensory symptoms, Positive sensory symptoms, Symptoms of autonomic dysfunction.
343
What are the causes, clinical features of spinal cord compression?
Causes: Vertebral tumors, disc and vertebral lesions, spinal cord tumors, inflammatory causes. Clinical Features: Spastic paraparesis, radicular pain, sensory loss.
344
What are the diagnosis & management of spinal cord compression?
Diagnosis: MRI to identify cause & site. Management: Urgent surgical decompression and stabilization.
345
What is syringomyelia and syringobulbia?
Fluid-filled cavity within the spinal cord or brainstem, caused by blockage of CSF flow or spinal cord trauma.
346
What are the clinical features, diagnosis, management of syringomyelia?
Cape-like distribution of sensory loss, loss of upper limb reflexes, muscle wasting, spastic paraplegia. Diagnosis: MRI.
347
What is Cauda Equina Syndrome?
Results from spinal damage at or distal to L1, most common cause is central lumbar disc prolapse.
348
What are the causes, clinical features, diagnosis, and treatment of transverse myelitis?
Acute inflammation of the cord affecting the whole cross-section. Causes: Immune-mediated process, infections. Clinical Features: Bilateral sensorimotor dysfunction. Diagnosis: MRI with contrast.
349
What is subacute combined degeneration of the spinal cord (SACD)?
Vitamin B12 deficiency. Clinical Features: Distal sensory loss, absent ankle jerks, exaggerated knee jerks.
350
What are the key features of Brown-Sequard syndrome?
Causes: Traumatic and non-traumatic. Clinical Features: Contralateral loss of pain and temperature, ipsilateral spastic hemiparesis.
351
What are the key features of anterior cord syndrome?
Traumatic/non-traumatic occlusion of the anterior spinal artery. Clinical Features: Complete paralysis below the level of the lesion, loss of pain and temperature sensation.
