Postsynaptic potentials

http://xa.yimg.com/kq/groups/6985863/1696231188/name/Neurophysiologic%20Basis%20of%20EEG-Olejniczak2006.pdf

http://jn.physiology.org/content/102/5/3046.full

Questions on EEG

1. What is electricity?
2. How do we measure it? 
3. What do we measure when we put an electrode on the scalp?
4. Obviously there is no movement of electrons across the electrodes, so it must be measuring some sort of a field. What is meant by electric field, how is it different from electromagnetic field and electrostatic field?

From www.physicsclassroom.com

Structure of matter

Not only do electrostatic occurrences permeate the events of everyday life, without the forces associated with static electricity, life as we know it would be impossible. Electrostatic forces - both attractive and repulsive in nature - hold the world of atoms and molecules together in perfect balance. Without this electric force, material things would not exist. Atoms as the building blocks of matter depend upon these forces. And material objects, including us Earthlings, are made of atoms and the acts of standing and walking, touching and feeling, smelling and tasting, and even thinking is the result of electrical phenomenon. Electrostatic forces are foundational to our existence.

Boyle's studies (middle to late 1600s) of gaseous substances promoted the idea that there were different types of atoms known as elements. Dalton (early 1800s) conducted a variety of experiments to show that different elements can combine in fixed ratios of masses to form compounds. Dalton subsequently proposed one of the first theories of atomic behavior that was supported by actual experimental evidence.

English scientist J.J. Thomson's cathode ray experiments (end of the 19th century) led to the discovery of the negatively charged electron and the first ideas of the structure of these indivisible atoms. Thomson proposed the Plum Pudding Model, suggesting that an atom's structure resembles the favorite English dessert - plum pudding. The raisins dispersed amidst the plum pudding are analogous to negatively charged electrons immersed in a sea of positive charge.

Nearly a decade after Thomson, Ernest Rutherford's famous gold foil experiments led to the nuclear model of atomic structure. Rutherford's model suggested that the atom consisted of a densely packed core of positive charge known as the nucleus surrounded by negatively charged electrons. While the nucleus was unique to the Rutherford atom, even more surprising was the proposal that an atom consisted mostly of empty space. Most the mass was packed into the nucleus that was abnormally small compared to the actual size of the atom.

Neils Bohr improved upon Rutherford's nuclear model (1913) by explaining that the electrons were present in orbits outside the nucleus. The electrons were confined to specific orbits of fixed radius, each characterized by their own discrete levels of energy. While electrons could be forced from one orbit to another orbit, it could never occupy the space between orbits.

Bohr's view of quantized energy levels was the precursor to modern quantum mechanical views of the atoms. The mathematical nature of quantum mechanics prohibits a discussion of its details and restricts us to a brief conceptual description of its features. Quantum mechanics suggests that an atom is composed of a variety of subatomic particles. The three main subatomic particles are the proton, electron and neutron. The proton and neutron are the most massive of the three subatomic particles; they are located in the nucleus of the atom, forming the dense core of the atom. The proton is charged positively. The neutron does not possess a charge and is said to be neutral. The protons and neutrons are bound tightly together within the nucleus of the atom. Outside the nucleus are concentric spherical regions of space known as electron shells. The shells are the home of the negatively charged electrons. Each shell is characterized by a distinct energy level. Outer shells have higher energy levels and are characterized as being lower in stability. Electrons in higher energy shells can move down to lower energy shells; this movement is accompanied by the release of energy. Similarly, electrons in lower energy shells can be induced to move to the higher energy outer shells by the addition of energy to the atom. If provided sufficient energy, an electron can be removed from an atom and be freed from its attraction to the nucleus.

Summary:

• All material objects are composed of atoms. There are different kinds of atoms known as elements; these elements can combine to form compounds. Different compounds have distinctly different properties. Material objects are composed of atoms and molecules of these elements and compounds, thus providing different materials with different electrical properties.
• An atom consists of a nucleus and a vast region of space outside the nucleus. Electrons are present in the region of space outside the nucleus. They are negatively charged and weakly bound to the atom. Electrons are often removed from and added to an atom by normal everyday occurrences. These occurrences are the focus of this Static Electricity unit.
• The nucleus of the atom contains positively charged protons and neutral neutrons. These protons and neutrons are not removable or perturbable by usual everyday methods. It would require some form of high-energy nuclear occurrence to disturb the nucleus and subsequently dislodge its positively charged protons. These high-energy occurrences are fortunately not an everyday event. One sure truth of this unit is that the protons and neutrons will remain within the nucleus of the atom. Electrostatic phenomenon can never be explained by the movement of protons.

Concepts in Static Electricity

Rubbing two objects against each other brings the electron fields of the atoms in each close to each other. Electron affinity varies amongst molecules. If there is a significant difference in this property between the two objects being rubbed against each other, then electrons will be transferred. This will result in a charge on the surface of both objects. The charge will obviously be of opposite polarity. It will also be equal in magnitude. This is known as the "Law of conservation of charge". A triboelectric series is the order in which objects are arranged according to the degree of electron affinity.

Dorsal digital expansion

Finger extension - DDE - 'Diamond' complex
1) Axis - Extensor digitorum tendon
2) Proximal wing tendon - interossei
3) Distal wing tendon - lumbricals
See Gray's Anatomy 37Ed Fig 5.70 5.71 5.83

Immunocompromising conditions

Immunocompromising Conditions (List from eMedicine)
a) Congenital
b) Acquired
c) Iatrogenic / self inflicted

a) Congenital Conditions

These most commonly affect the fetus and newborn. Hemoglobinopathy may be noted.
Syndromes

• Partial albinism with immunodeficiency (Griscelli) syndrome^{[2, 3]}
• Hemorrhagic hereditary telangiectasia (Rendu-Osler disease)^[4]
• Immunodeficiency-centromeric instability-facial anomalies (ICF) syndrome
• Kabuki syndrome
• Partial albinism, immunodeficiency, and progressive white matter disease (PAID) syndrome
• Autoimmune polyendocrinopathy syndrome type 1
• Rubinstein-Taybi syndrome^[5]
• Hermansky-Pudlak-2 syndrome
• CHARGE syndrome^[6]
• Other dysmorphology or immunodeficiency syndromes
• Stromal interaction molecule 1 mutation^[7]

B-cell defects^[8]

• Antibody deficiency with transcobalamin II deficiency
• Antibody deficiency with normal or high immunoglobulin (Ig) levels
• Common variable immunodeficiency
• IgG heavy-chain deletion
• IgG subclass deficiency
• Kappa-chain deficiency
• Organic cation transporter 2 deficiency
• Selective IgA deficiency
• Selective IgM deficiency
• Selective antipolysaccharide antibody deficiency
• Transient hypogammaglobulinemia of infancy or early childhood
• Thymoma with agammaglobulinemia
• X-linked (Bruton) agammaglobulinemia
• X-linked hyper-IgM syndrome
• X-linked hypogammaglobulinemia with growth hormone deficiency

Combined B-cell and T-cell defects

• Adenosine deaminase deficiency
• Artemis deficiency
• Ataxia-telangiectasia syndrome
• Bare lymphocyte syndrome (major histocompatability complex class I/II deficiency)
• DOCK8 mutations^[9]
• Interleukin (IL)-2R alpha or gamma deficiency
• Intestinal lymphangiectasia
• Janus kinase 3 (JAK3) deficiency
• Nuclear factor-kappaB essential modifier (NEMO) deficiency (Dupuis-Girod, 2002; Courtois, 2006; Smahi, 2002; Zonana, 2000)
• Nijmegen breakage syndrome
• Omenn syndrome
• Purine nucleoside phosphorylase deficiency
• Recombination activation gene (RAG) 1 or 2 deficiency
• Reticular dysgenesis
• Swiss-type severe combined immunodeficiency
• T-cell receptor deficiency
• Wiskott-Aldrich syndrome^[10]
• X-linked lymphoproliferative syndrome
• X-linked severe combined immunodeficiency
• Zeta-associated protein of 70 kDa (ZAP-70) tyrosine kinase deficiency

T-cell defects

• Biotin-dependent multiple carboxylase deficiency
• Chronic mucocutaneous candidiasis
• DiGeorge (velocardiofacial) syndrome
• Fas defect
• Nezelof syndrome
• Short-limbed dwarfism or cartilage-hair hypoplasia

Macrophage, cytokine, and miscellaneous defects

• Mendelian susceptibility to mycobacterial diseases (MSMD)
  

  • Interferon-gamma deficiency
  • Interferon-gamma receptor I or II deficiency
  • IL-12 deficiency
  • IL-12 receptor deficiency
  • STAT1 mutations
  • NEMO
  • CYBB
• IL-1 receptor–associated kinase 4 (IRAK4) deficiency
• MYD88 deficiency
• Toll-like receptor 5 mutations
• Apolipoprotein L-I deficiency
• UNC-93B deficiency
• Toll-like receptor 3 mutations
• TRIF and TRAF3 mutations
• Plasminogen activator inhibitor-1 4G/4G promoter genotype
• Anti-interferon-gamma antibodies
• IL-18 polymorphisms
• RANTES promoter gene polymorphisms^[11]
• Deficiency of chemokine receptor CCR5^{[12, 13]}
• Toll-like receptor 4 mutations
• IL-8 RA (chemokine CXC motif receptor 1 [CXCR1]) mutations
• CXCR4 mutations (Whim syndrome)
• STAT 5 mutations
• NOD2 gene polymorphisms
• IL-6 polymorphisms
• Activating killer immunoglobulinlike receptor gene polymorphisms
• Dectin-1 deficiency
• CARD9 mutations
• Polymorphisms in cytokine-inducible SRC homology 2 domain protein (CISH)
• Polymorphisms in Mal/TIRAP and Interleukin-10
• Autoantibodies against IL-6^[14]
• Polymorphisms in the IL-8 promoter gene^[15]
• IL-12 receptor deficiency (Vinh, 2011)

Phagocyte deficiency or dysfunction

• Chediak-Higashi syndrome
• Chronic granulomatous disease
• Chronic idiopathic neutropenia
• Cyclic neutropenia
• Glycogen storage disease 1b
• Hyper-IgE/recurrent infection (Job) syndrome (Janus kinase protein tyrosine kinase 2 [Tyk2], signal transducer and activator of transcription [STAT] 3, and STAT 1 mutations)^[16]
• Kostmann syndrome
• Leukocyte adhesion deficiency (including CD11 or CD18 deficiency)
• Myeloperoxidase deficiency
• Neutrophil actin dysfunction
• Papillon-Lefèvre syndrome
• Specific granule deficiency
• Shwachman-Diamond syndrome

Complement deficiencies (Ram, 2010)

• Mannose-binding lectin (Mannan-binding protein) deficiency^{[17, 18]}
• Deficiencies of C1q, C1r, C1rs, C4, C2, C3, or C5-9
• Deficiencies of factor D, factor P, factor I, factor H, or properdin
• Ficolin-3 (H-ficolin) deficiency^[19]

Other conditions

• Asplenia^[20]
• Ciliary dyskinesia, Kartagener syndrome, and other disorders
• Galactosemia and other metabolic conditions
• Lymphedema (congenital)
• Trisomy 21 and other genetic disorders
• Other anatomic defects (eg, midline dermal sinus, Mondini defect of the inner ear, fistulae, cysts, duplications, meningeal defects, iron overload, decreased sensation)

b) Acquired Conditions

These conditions may interfere directly with the immune system or may disrupt barrier function.

• Malnutrition
• HIV infection: Although human immunodeficiency virus (HIV) infection is a considerable cause of immunodeficiency worldwide, immunocompromise is most likely to result from common problems, including asthma, diabetes, malnutrition, and cancer, among others.
• Trauma
  

  • Burns
  • Lacerations and abrasions
• Medical conditions
  

  • Collagen vascular
  • GI tract
  • Hematologic or oncologic
  • Hepatic
  • Metabolic
  • Pregnancy
  • Pulmonary, particularly asthma and cystic fibrosis (CF)
  • Renal
  • Skin and mucous membrane
  • Viral infections (eg, cytomegalovirus [CMV] infection,^[21] measles)
  • Other anatomic or physiologic problems (eg, fistulae, cysts, obstructions, iron overload, decreased sensation)
• Acquired asplenia (Ram, 2010)
• Acquired lymphedema
• Other conditions that injure or bypass barrier function
  

  • Parasitic infections
  • Animal and insect bites or scratches

c) Iatrogenic or Self-inflicted Conditions

These conditions may directly interfere with the immune system or may disrupt barrier function.
Use of drugs and/or therapies (eg, radiation therapy), which may interfere with normal flora, decrease gastric acidity and ciliary motility, and be directly immunomodulating^[22]
Trauma

• Injections (eg, insulin injections, intravenous [IV] drug use, others)
• Operative and other incisions
• Vascular, osseous, tracheal, gastric, bladder, joint, peritoneal, wound, or ventricular access or drainage devices
• Internal foreign bodies
• Major surgery^[23]

Treatment

• For leukemia or lymphoma
• Bone marrow or stem-cell transplantation
• Solid organ transplantation (Yin, 2011)
• Therapy for autoimmune or inflammatory disorders
• TNF-alpha inhibitors^[24]
• Monoclonal antibodies and related small molecules

Wilsons disease with behavioral problems and isolated midbrain lesions

Question - can patients with Wilsons disease present with isolated psychopathic (especially abnormal sexual) behavior?
Yes - see the range of behavioral manifestations in Wilsons http://neuro.psychiatryonline.org/data/Journals/NP/3960/08JNP81.PDF , http://www.ncbi.nlm.nih.gov/pubmed/7872138 , http://books.google.co.in/books?id=Ag5710EHVpAC&pg=PA23&lpg=PA23&dq=wilsons+disease+substance+abuse&source=bl&ots=63ocZTdPcm&sig=L0H9HbqTcqwIGw-NFNk6j1iklvw&hl=en&sa=X&ei=pCyiUKH4AY7trQf0m4DoBw&ved=0CE4Q6AEwBQ#v=onepage&q=wilsons%20disease%20substance%20abuse&f=false

Question - can patients with Wilsons disease have changes only in midbrain (no changes in putamen / lenticular nuclei)
Yes - see the range of MRI abnormalities in Wilsons http://www.ncbi.nlm.nih.gov/pubmed/17894614 , http://www.ncbi.nlm.nih.gov/pubmed/20437536 , http://www.ncbi.nlm.nih.gov/pubmed/16752136

Question - can patients with Wilsons disease have only abnormality of elevated 24 hour urinary copper?
Yes - see the range of biochemical abnormalities and guidelines for diagnosis of Wilsons disease http://www.uptodate.com/contents/tests-used-in-the-diagnosis-of-wilson-disease , http://guidelines.gov/content.aspx?id=13004

Wilsons Behavioral Problems 1995 article

http://www.ncbi.nlm.nih.gov/pubmed/7872138

Adv Neurol. 1995;65:171-8.
Psychiatric and behavioral abnormalities in Wilson's disease.
Akil M, Brewer GJ.Department of Psychiatry, University of Pittsburgh, Western Psychiatric Institute and Clinic, Pennsylvania 15213.

From the literature and our experience, a relatively consistent picture of psychiatric and behavioral abnormalities in Wilson's disease emerges. The essential elements of this picture are as follows: 

1. Psychiatric and behavioral abnormalities are frequent manifestations of WD. The estimates range from 30% (18) to 100% (2) of symptomatic patients. As Wilson himself was the first to state in reference to "mental change," "its importance should not be underestimated." 

2. Psychiatric and behavioral abnormalities are often the initial manifestations of WD. Two thirds of our patients first presented with psychiatric symptoms and one third received psychiatric treatment before the diagnosis of WD was made. In the early stages of the disease, when psychiatric and behavioral symptoms predominate, the diagnosis is often missed. Of our 124 patients, WD was diagnosed in only one during this phase. Until the psychiatric presentation of WD is recognized, and the disease is included in the differential diagnosis of psychiatric symptoms, its diagnosis will be missed or delayed. In our patients, and others' (13,15), the delay in diagnosis ranged from 1 to 5 years. Such a delay is particularly tragic as favorable outcome depends upon early discovery. 

3. The most common of the psychiatric and behavioral manifestations of WD include: personality changes such as irritability and low threshold to anger, depression sometimes leading to suicidal ideation and attempts, deteriorating academic and work performance that is present in almost all neurologically affected patients. We (1) have also observed, as did Scheinberg and Sternlieb (2) that WD patients exhibit increased sexual preoccupation and reduced sexual inhibition. Finally, cognitive impairment, psychosis, anxiety, and other psychiatric disorders, although less frequent, also occur. 

4. Some of the psychiatric and behavioral symptoms are reversible with WD-specific therapy, whereas others are not. We are impressed with the frequency with which the behavioral and "cognitive" symptoms are reversed over 1 to 2 years of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Violence and psychopathic behavior presentation

Neurological and systemic conditions listed on various websites including Crime Times

1. Temporal lobe/ amygdala lesions - tumors, HSE
2. Toxins like organophosphates and carbamates
3. Thyroid disorders
4. Wilsons disease, Huntington's disease, hyperparathyroidism, vitamin deficiencies, limbic encephalitis, and sleep disorders

Conditions associated with sex offences - Tourette's syndrome (anecdotal response of abnormal sexual behavior to pimozide) and Wilson's disease

Retinal Vasculitis with CNS disease

In a patient with retinal vasculitis, it is useful to know the following:
1) Type of retinal vessels involved - arterioles, venules, capillaries
2) CSF study normal or abnormal
3) MRI Brain normal, vasculitis, white matter changes, ventricular enlargement

Identification of retinal vessels involved 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2855661/

Retinal vasculitis affecting predominantly the veins (phlebitis) has been described in association with Behçet's disease, tuberculosis, sarcoidosis, multiple sclerosis, pars planitis, retinal vasculitis associated with tuberculoprotein hypersensitivity (Eales' disease), human immunodeficiency virus infection (HIV). Retinal arteritis is more commonly seen in acute retinal necrosis, idiopathic retinal vasculitis, aneurysms, and neuroretinitis (IRVAN) and systemic vasculitides such as SLE, polyarteritis nodosa, and Wegener's granulomatosis, Churg-Strauss syndrome and cryoglobulinemia.

List of causes of retinal vasculitis (Uptodate)

Systemic disorders

Behcet's disease

Granulomatosis with polyangiitis (Wegener's)

Sarcoidosis

Relapsing polychondritis

Systemic lupus erythematosus

Giant cell arteritis

Polyarteritis nodosa

Multiple sclerosis

Whipple's disease

Crohn's disease

HLA-B27 associated conditions

Infectious disorders

Toxoplasmosis

Tuberculosis

Syphilis

Herpes simplex

Herpes zoster

Acute retinal necrosis

Cytomegalovirus

Coccidiomycosis

Hepatitis

Amoebiasis

Candidiasis

Leptospirosis

Ricketsia

Brucellosis

Lyme disease

Human immunodeficiency virus

Toxocariasis

Ocular disorders

Birdshot retinochoroidopathy

Pars planitis

Eale's disease

Retinal arteriolitis

Behcet's sine systemic disease

Sympathetic ophthalmia

Classification of retinal vasculitis by involved vessel

Disease	Primary vessel involved
Polyarteritis nodosa	Muscular arteries
Granulomatosis with polyangiitis (Wegener's); giant cell arteritis	Medium to small arteries
Systemic lupus erythematosus	Small arteries
Whipple's disease	Capillaries
Behcet's disease; sarcoidosis; multiple sclerosis	Veins
Crohn's disease; relapsing polychondritis	Arteries and veins
HLA-B27 associated conditions, such as ankylosing spondylitis	Variable or no involvement

EEG Questions

What is the electrical principle behind an EEG?

What is actually moving (?electrons), why is it moving, and how do we pick up the amount and direction of movement?

What is the relation between movement of electrons and electrical field?

What are the electrodes on the surface of the scalp actually picking up?

How is the electric field in scalp recording different from ECG?

What is really meant by potential difference?