Sites causing Ataxic Hemiparesis

Sites causing Ataxic Hemiparesis

1. C/L thalamocapsular
2. C/L posterior limb of internal capsule
3. C/L red nucleus
4. C/L basis pontis- juntion of upper third and lower two thirds
5. Superficial ACA supplying paracentral area

Sites of Dysarthria- Clumsy Hand Syndrome

Sites of Dysarthria- Clumsy Hand Syndrome

1. Genu of internal capsule
2. Small deep cerebellar hemorrhage
3. Basis pontis at junction of upper third and lower two third

Sites of Pure Motor Hemiparesis

Sites of Pure Motor Hemiparesis

A. Intracranial-
1. Posterior limb of Internal Capsule
2. Cerebral Peduncle
3. Medullary pyramid.
4. Basis pontis 

House-Brackmann scale

The House-Brackmann scale is a facial nerve grading system, at one end of the scale there is normal facial nerve function and at the other there is complete paralysis.

Grade	FunctionLevel	Symmetry at Rest	Eye(s)	Mouth	Forehead
I	Normal	Normal	Normal	Normal	Normal
II	Mild	Normal	Easy and complete closure	Slightly asymmetrical	Reasonable function
III	Moderate	Normal	With effort, complete closure	Slightly affected with effort	Slight to Moderate movement
IV	Moderately Severe	Normal	Incomplete closure	Asymmetrical with maximum effort	None
V	Severe	Asymmetry	Incomplete closure	Minimal Movement	None
VI	Total Paralysis	Total Paralysis

Complications of IvIg infusion

Nephrotic syndrome
Aseptic meningitis
Serum sickness
Thrombotic venous/arterial occlusion
Stroke
Hypotension

Wernicke's Encephalopathy- non alcoholic causes

prolonged intravenous feeding,

hyperemesis gravidarum, 

anorexia nervosa, 

refeeding after starvation, 

thyrotoxicosis, 

regional enteritis, 

malabsorption syndromes, 

hemodialysis, 

peritoneal dialysis,

uremia, 

HIV,

malignancy, and 
gastroplasty with postoperative vomiting

Hughes GBS Disability Scale

Guillain-Barré Syndrome Disability Scale (Hughes)

0	Healthy
1	Minor symptoms or signs of neuropathy but capable of manual work/capable of running
2	Able to walk without support of a stick (5m across an open space) but incapable of manual work/running
3	Able to walk with a stick, appliance or support (5m across an open space)
4	Confined to bed or chair bound
5	Requiring assisted ventilation (for any part of the day or night)
6	Death

Asbury Criteria for GBS

Diagnostic criteria
Assessment of current diagnostic criteria for Guillain-Barre syndrome

Required features

• Progressive weakness in both arms and legs
• Areflexia (or hyporeflexia).

Features supportive of diagnosis

• Progression of symptoms over days to 4 weeks
• Relative symmetry
• Mild sensory signs or symptoms
• Cranial nerve involvement, especially bilateral facial weakness
• Recovery beginning 2 to 4 weeks after progression ceases
• Autonomic dysfunction
• Absence of fever at onset
• Typical CSF (albuminocytologic dissociation)
• EMG/nerve conduction studies (characteristic signs of a demyelinating process in the peripheral nerves)

Features casting doubt on the diagnosis

• Asymmetrical weakness
• Persistent bladder and bowel dysfunction
• Bladder or bowel dysfunction at onset
• >50 mononuclear leukocytes/mm³ or presence of polymorphonuclear leukocytes in CSF
• Distinct sensory level.

Features that rule out the diagnosis

• Hexacarbon abuse
• Abnormal porphyrin metabolism
• Recent diphtheria infection
• Lead intoxication
• Other similar conditions: poliomyelitis, botulism, hysterical paralysis, toxic neuropathy.

Uses of phenytoin



Phenytoin is used as both an abortive and preventive medication in seizure management. Intravenous administration of phenytoin ceased seizure activity in 60%-80% of patients in status epilepticus within 20 minutes. Prophylactic indications include pregnancy-induced hypertension, postneurosurgery, cerebrovascular accidents, and traumatic brain injury. Of these, there is inconsistent evidence to support the routine use of phenytoin in patients who have undergone craniectomy.

Less-common uses of phenytoin include the treatment of neuropathic pain, motion sickness, muscular dystrophy, and arrhythmia.

Phenytoin levels



Phenytoin is used as both an abortive and preventive medication in seizure management.
The total phenytoin reference range varies by age, as follows:

• Children and adults: 10-20 µg/mL
• Neonates: 8-15 µg/mL

Toxic phenytoin levels are defined as greater than 30 µg/mL.
Lethal levels are defined as greater than 100 µg/mL.
The reference range of free phenytoin is 1-2.5 µg/mL.
In patients with renal failure associated with hypoalbuminemia, free phenytoin levels may be more accurate than total phenytoin levels.However, the Sheiner-Tozer formula (below) can be used to correct the phenytoin level.
Adjusted concentration = measured total concentration / [(0.2 x albumin) + 0.1].
Administration of phenytoin and interpretation of serum phenytoin levels vary depending on the clinical scenario. Loading doses to achieve rapid therapeutic levels should be checked 1 hour after an intravenous loading dose and 24 hours after an oral loading dose.
Patients who are on long-term phenytoin therapy generally do not need to be monitored at intervals less than 3-12 months after a steady state has been reached unless clinically indicated, for example in patients who may have intentionally or unintentionally taken a toxic dose.
Although the reference range is between 10 and 20 µg/mL, about half of patients’ seizures are controlled at values lower and higher than the therapeutic range.
Some adverse effects of phenytoin are related to specific serum levels. Nystagmus is frequently observed at levels greater than 20 µg/mL.At greater than 30 µg/mL, patients may exhibit slurring of speech, ataxia, and movement disorders such as tremor, choreoathetosis, and orofacial dyskinesia.At serum levels that exceed 40 µg/mL, patients are often lethargic, stuporous, and confused and may require aggressive supportive measures.

Anatomy of Speech

Language processes have a clear neuroanatomical basis. 

In simplest terms, the reception and processing of spoken language take place in the auditory system, beginning with the cochlea and proceeding through a series of way stations to the auditory cortex, the Heschl gyrus, in each superior temporal gyrus. Decoding sounds into linguistic information involves the posterior part of the left superior temporal gyrus, the Wernicke area or Brodmann area 22, which gives access to a network of cortical associations to assign word meanings. For both repetition and spontaneous speech, auditory information is transmitted to the Broca area in the posterior inferior frontal gyrus. This area of cortex “programs” the neurons infrom which descending axons travel to the brainstem cranial nerve nuclei. The inferior parietal lobule, especially the supramarginal gyrus, also may be involved in phoneme processing in language comprehension and in phoneme production for repetition and speech. 

Reading requires perception of visual language stimuli by theoccipital cortex, followed by processing into auditory language information via the heteromodal association cortex of the angular gyrus. Writing involves activation of motor neurons projecting to the arm and hand.

Lateral Ventricle- Parts

There are several areas in the lateral ventricle:
• the frontal horn, which is bounded by the caudate nucleus, Corpus callosum and septum pellucidum
• the body of the lateral ventricle is bounded by the caudate nucleus / thalamus, corpus callosum and fornix
• the atrium: this is the focal point of the occipital and temporal horns
• the occipital horn
• the temporal horn

The two lateral ventricles (right, left) communicate with each other via the third ventricle.

P

Etiological Classification of seizures

The classification (database) of etiologies of the epilepsies is divided into four main categories.

Definitions

1. Idiopathic epilepsy—defined here as an epilepsy of predominately genetic or presumed genetic origin and in which there is no gross neuroanatomic or neuropathologic abnormality. Included here are epilepsies of presumed multigenic or complex inheritance, but for which currently the genetic basis has not been elucidated.

2. Symptomatic epilepsy—defined here as an epilepsy of an acquired or genetic cause, associated with gross anatomic or pathologic abnormalities, and/or clinical features, indicative of underlying disease or condition. We thus include in this category developmental and congenital disorders where these are associated with cerebral pathologic changes, whether genetic or acquired (or indeed cryptogenic) in origin. Also included are single gene and other genetic disorders in which epilepsy is

only one feature of a broader phenotype with other cerebral or systemic effects.

3. Provoked epilepsy—defined here as an epilepsy in which a specific systemic or environmental factor is the predominant cause of the seizures and in which there are no gross causative  neuroanatomic or neuropathologic changes. Some ‘‘provoked epilepsies’’ will have a genetic basis and some an acquired basis, but in many no inherent cause can be identified. The reflex epilepsies are

included in this category (which are usually genetic) as well as the epilepsies with a marked seizure precipitant.

4. Cryptogenic epilepsy—defined here as an epilepsy of presumed symptomatic nature in which the cause has not been identified. The number of such cases is diminishing, but currently this is still an important category, accounting for at least 40% of adult-onset cases of epilepsy.

ABCD2 SCALE- TIA

Memory

Procedural memory is a part of the long-term memory that is responsible for knowing how to do things, also known as motor skills. As the name implies, procedural memory stores information on how to perform certain procedures, such as walking, talking and riding a bike.  Procedural memory is sometimes referred to as implicit memory, because previous experiences aid in the performance of a task without explicit and conscious awareness of these previous experiences, although it is more properly a subset of implicit memory.

Declarative memory (“knowing what”) is memory of facts and events, and refers to those memories that can be consciously recalled (or "declared"). It is sometimes called explicit memory, since it consists of information that is explicitly stored and retrieved, although it is more properly a subset of explicit memory. Declarative memory can be further sub-divided into episodic memory and semantic memory.

Episodic memory is the memory of autobiographical events (times, places, associated emotions, and other contextual who, what, when, where, why knowledge) that can be explicitly stated. It is the collection of past personal experiences that occurred at a particular time and place.

Neurological Laws

Alexander's law refers to the phenomenon in which the spontaneous nystagmus of a patient with a vestibular lesion is more intense when the patient looks in the quick-phase than in the slow-phase direction. 

Forearm ischemic exercise screening test

There is evidence that ischemic exercise test can be harmful in patients with myopathies. Therefore recently non-ischemic forearm exercise test has been suggested. However in view of the long tradition of ischemic testing and the lack of sensitivity in mitochondrial myopathy the protocol for ischemic testing is given.

While the patient is at rest, blood samples are taken for baseline levels of lactate and ammonia. A blood pressure cuff is then placed over the upper arm and inflated to a pressure higher than systolic, rendering the forearm ischemic. The patient begins immediately repetitive, rapid grip exercises. Normal individuals are able to tolerate ischemic exercise for as long as 180 seconds before pain and fatigue ensues. Patients with glycogen metabolism disorders seldom exercise more than 60 seconds.

When the patient fatigues, the blood pressure cuff is released and 1 minute later blood is drawn from the exercised arm. Similar samples are taken again at 2,4,6,10,and 14 minutes following the end of the exercise.

Normal subjects exhibit a 3 to 5 fold rise in lactate and ammonia levels within 5 minutes after the end of the exercise, with a full return to baseline level about 10-15 minutes after cessation of the test. Failed lactate production suggest a metabolic block (myophosphorylase deficiency (McArdle disease)). The venous level of ammonia also rises during the test. Failure of the lactate and ammonia to rise suggests an inadequate test. Normal lactate but impaired ammonia production suggests myoadenylate deaminase deficiency or a related disorder of purine nucleotide metabolism.

Charcot-Bouchard aneurysms

Charcot-Bouchard aneurysms are a common cause of stroke. If a Charcot-Bouchard aneurysm ruptures, it will lead to an intracerebral hemorrhage.

• French physicians Jean-Martin Charcot and Charles-Joseph Bouchard described it. Bouchard discovered these aneurysms.
• Charcot-Bouchard aneurysms are associated with chronic hypertension.
• They are usually occur due to involvement of small penetrating (<300 µm) lenticulostriate branch of middle cerebral artery in the basal ganglia, brainstem and midbrain.

They are the reason why hypertensive bleed is most common in Basal Ganglia

Stiff Person Syndrome- Antibodies

The most common pathologic correlate is anti–glutamic acid decarboxylase (GAD) antibodies (It has been associated with a wide range of neurologic diseases). 

Additional possible pathophysiologic etiologies in patients negative for GAD antibody include postsynaptic elements such as synaptophysin, amphiphysin, gephyrin, and GABA-transaminase. 

It is also associated with a number of non-neurologic diseases, including diabetes mellitus and thyroiditis.

NOS

A dissociate disorder NOS (Not Otherwise Specified) is a disorder that includes a dissociative symptom (i.e., a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment) that does not meet the criteria for any specific Dissociative Disorder. This disorder is no longer recognized in the 2013 DSM-5 and exists now for informational/historical purposes.

Examples-

• Presentations in which a) there are not two or more distinct personality states, or b) amnesia for important personal information does not occur.
• Derealization unaccompanied by depersonalization in adults.
• States of dissociation that occur in individuals who have been subjected to periods of prolonged and intense coercive persuasion (e.g., brainwashing, thought reform, or indoctrination while captive).
• Dissociative trance disorder: single or episodic disturbances in the state of consciousness, identity, or memory that are indigenous to particular locations and cultures. Dissociative trance involves narrowing of awareness of immediate surroundings or stereotyped behaviors or movements that are experienced as being beyond one’s control. Possession trance involves replacement of the customary sense of personal identity by a new identity, attributed to the influence of a spirit, power, deity, or other person, and associated with stereotyped “involuntary” movements or amnesia. Examples include amok (Indonesia), bebainan (Indonesia), latah (Malaysia), pibloktoq (Arctic), ataque de nervios (Latin America), and possession (India). The dissociative or trance disorder is not a normal part of a broadly accepted collective cultural or religious practice. 
• Loss of consciousness, stupor, or coma not attributable to a general medical condition.
• Ganser syndrome: the giving of approximate answers to questions (e.g., “2 plus 2 equals 5″) when not associated with Dissociative Amnesia or Dissociative Fugue.