Download Neuro examination algorithm: 1. Meningeal irritation signs: • Neck

Neuro examination algorithm: 1. Meningeal irritation signs: • Neck stiffness: Nuchal rigidity is the inability to flex the head forward due to rigidity of the neck muscles • Kernig sign: elevation of the extended lower extremities cause a sudden flexion of the knee. • Brudzinski sign: involuntary lifting of the legs in meningeal irritation when lifting a patient's head off the examining couch. 2. Cranial nerves: • I., Olfactory nerve: hyposmia, anosmia (szaglásával van probléma?) • II., Confrontal visual field examination. Pupillary reflex (II-­‐III). Visus. • III-­‐IV-­‐VI., Eye movements: full range, limitation? (Kövesse a tollam hegyét, fejét ne mozgassa!) o Occulomotor paresis: eye bulb is out and downward, pupil dilated, ptosis. o Trochlear nerve paresis: eye bulb is in and upward. Head tilted. o Abducent nerve paresis: eye bulb is inward. Head turned. o Internuclear ophtalmoparesis: lesion of the fasciculus longitudinalis medialis o Nystagmus (direction: direction of the fast component. 1st, 2nd, 3rd degree). o Pupils: isocoria, anisocoria, mydriasis, miosis. o Accomodation o Pupillary light reflex • V., Compare light touch sensation on the two sides of the face according to the three branches (Egyformán érzi a két oldalon?). Cornea reflex. (Carefull!) • VII., Central, peripheral facial palsy. Watch for the forehead! (Csücsörít, vicsorít, homlokát ráncolja) • VIII., Weber -­‐ lateralisation? (Melyik fülével halja hangosabban?), Rinne -­‐ positive is good! (Szóljon ha már nem halja!) • XI., Agenusia on the posterior third (Ízérzéssel van gond?). Diminution of gag and palatal reflexes. Dysphagia (Nyeléssel van gond? Szilárd, folyékony?) • X., Missing gag reflex, soft palete hangs down. Nasal speech. Palatal veil pulled over to the normal side when phonating (Mondja azt, hogy "A"). Hoarseness. Dysphagia. Tachycardia. • XI., Shoulder drop (Emelje fel a vállát!). Weakness of turning the head (Fordítsa a fejét!) • XII., Protruded toung deviate to the side of the lesion. (Öltse ki a nyelvét!) Supranuclear lesions produces no significant deficit of the tounge motility (bilateral innervation). 3. Muscle tone (rigidity vs. spasticity) (Lazítsa el!) Hypertonia can be either spasticity or rigidity. Spasticity is from a UMN lesion. It is rate dependent resistance on range of motion with collapse of the resistance at the end of the range of motion. This is called the clasp-­‐
knife phenomena. Rigidity is from basal ganglia disease. The resistance to range of motion is not rate or force dependent and is constant throughout the range of motion. This is often referred to as lead pipe or plastic-­‐like rigidity. Check for cog-­‐wheel sign. Watch for agonists and antagonists! 4. Paresis: raise hands (45 degree, palms up) and legs (flexed in hip and knee 90 degree) Emelje fel mindkét kezét, tenyérrel felfele, csukott szemmel tartsa meg! Lábát behajlítva emelje fel, ne érjen össze, csukott szemmel tartsa meg! • Degree: o 0/5: No muscle movement o 1/5: Visible muscle movement, but no movement at the joint o 2/5: Movement at the joint, but not against gravity o 3/5: Movement against gravity, but not against added resistance (drift against gravity) o 4/5: Movement against resistance, but less than normal o 5/5: Normal strength • movements to test: o Flexion at the elbow (C5, C6, biceps) o Extension at the elbow (C6, C7, C8, triceps) o Extension at the wrist (C6, C7, C8, radial nerve) o Squeeze two of your fingers as hard as possible ("grip," C7, C8, T1) o Finger abduction (C8, T1, ulnar nerve) o Abduction/oppostion of the thumb (C8, T1, median nerve) o Flexion at the hip (L2, L3, L4, iliopsoas) o Adduction at the hips (L2, L3, L4, adductors) o Abduction at the hips (L4, L5, S1, gluteus medius and minimus) o Extension at the hips (S1, gluteus maximus) [12] o Extension at the knee (L2, L3, L4, quadriceps) [10] o Flexion at the knee (L4, L5, S1, S2, hamstrings) o Dorsiflexion at the ankle (walk on wheels; L4, L5, peroneal nerve) o Plantar flexion (tip-­‐toe; S1, tibial nerve) 5. Deep tendon reflexes (areflexia, hyporeflexia, normal, brisk reflex, hyperreflexia-­‐extended reflexogen zone, clonus) • Biceps (C5, C6) o The patient's arm should be partially flexed at the elbow with the palm down. o Place your thumb or finger firmly on the biceps tendon. o Strike your finger with the reflex hammer. o You should feel the response even if you can't see it. • Triceps (C6, C7) o Support the upper arm and let the patient's forearm hang free. o Strike the triceps tendon above the elbow with the broad side of the hammer. o If the patient is sitting or lying down, flex the patient's arm at the elbow and hold it close to the chest. • Brachioradialis (C5, C6) o Have the patient rest the forearm on the abdomen or lap. o Strike the radius about 1-­‐2 inches above the wrist. o Watch for flexion and supination of the forearm. • Abdominal (T8, T9, T10, T11, T12) o Use a blunt object such as a key or tongue blade. •
•
o Stroke the abdomen lightly on each side in an inward and downward direction above (T8, T9, T10) and below the umbilicus (T10, T11, T12). o Note the contraction of the abdominal muscles and deviation of the umbilicus towards the stimulus. Knee (L2, L3, L4) o Have the patient sit or lie down with the knee flexed. o Strike the patellar tendon just below the patella. Start from below tapping the tibia. o Note contraction of the quadriceps and extension of the knee. Ankle (S1, S2) o Dorsiflexion the foot at the ankle. o Strike the Achilles tendon. o Watch and feel for plantar flexion at the ankle. 6. Pathologic reflexes (cortico-­‐spinal injury): • Extension of the toe: o Babinski´s sign: Stroke the lateral aspect of the sole with the plastic cover of a needle. Normally: flexion of the toe (withdrawal). Positive: slow tonic extension of the big toe with fanning of the other toes. o Chaddock´s sign: scratching the skin over the lateral malleolus. o Oppenheim´s sign: stroking downward along the medial side of the tibia • flexion of the toes: o Rossolimo´s sign: plantar flexion of the toes on tapping their plantar surface o Mendel-­Bechtěrev´s sign: dorsal flexion of the second to fifth toes on percussion of the dorsum of the foot • Upper extremity: o Hoffmann’s sign: a sudden nipping of the nail of the index, middle, or ring finger produces flexion of the terminal phalanx of the thumb and of the second and third phalanges of some other finger. o Trömner’s sign: flexion of the thumb and index finger in response to tapping or flicking the volar surface of the distal phalanx of the middle finger, held partially flexed between the examiner’s finger and thumb. o Inverse radial reflex: flexion of the fingers without flexion of the forearm, on tapping the lower end of the radius 7. Coordination and cerebellar signs • Finger to nose, heel to knee test o Ataxia: inability to coordinate muscle activity during voluntary movement o Dysmetria: An aspect of ataxia, in which the ability to control the distance, power, and speed of an act is impaired o Dysdiadochokinesis: Inability to perform rapid alternating movements o Intention tremor: tremor that occurs during the performance of precise voluntary movements Romberg test: Stand erect with feet together and eyes closed. Positive: swaying to specific direction or irregular swaying and even toppling. Check with eyes open and closed. Note: balance needs one of the two: proprioception or vision. If get worse when eyes closed suggests deficiency of proprioception. If visual input does not make a difference cerebellar lesion is expected. • Barany pointing test: the patient points at a fixed object (the examiners fingers) alternately with the eyes open and closed; a constant error with the eyes closed indicates a cerebellar lesion on the ipsilateral side. • Nystagmus: biphasic ocular oscillation alternating a slow eye movement, or smooth pursuit, in one direction and a fast eye movement, or saccadic movement, in the other direction. Named after the fast component. The slow movement is the pathologic. o Opticokinetic nystagmus. A nystagmus induced by looking at moving visual stimuli, such as moving horizontal or vertical lines, and/or stripes. o Postrotatory nystagmus. If one spins in a chair continuously and stops suddenly, the fast phase of nystagmus is in the opposite direction of rotation o Vestibular nystagmus: slow component is in the direction of the lesioned vestibular organ. Comes with certain latency after the head movement. The direction of fall in Romberg and the deviation in Bárány test is opposite to the direction of the nystagmus (fast component): harmonic syndromes. o Central nystagmus: More likely being rotational. Attenuated by closing the eyes. The direction of fall in Romberg and the deviation in Bárány is the same as the fast component of the nystagmus. Usually comes with other brain stem symptoms. • Scanning speech: abnormal speech characterized by a staccato-­‐like articulation in which the words are clipped and broken because the person pauses between syllables • Charcot triad: scanning speech, intention tremor, nystagmus. • Cerebellar hypotonia: muscle tone is reduced ipsilateral to the side of the cerebellar lesion. 8. Extrapyramidal system • Bradykinesia: slowness of initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions • Rigidity: increased muscle tone, equal in flexors and extensors, and may feel like bending a lead pipe; the presence of additional tremor (which may not be visibly evident) can add a ‘cogwheel’ feel • Rest tremor: 4-­‐6Hz, pill-­‐rolling, subside with movement, reappear after an interval when a new position of rest • Postural instability • Chorea: excessive spontaneous movements, irregularly timed, randomly distributed and abrupt. Severity may range from restlessness with mild intermittent exaggeration of gesture and expression, fidgety movements of the hands or unstable dance-­‐like gait to a continuous flow of disabling and violent movements. •
o … 9. Sensory system • Spinothalamic system: o Heat sensation (investigate with hot or cold tube) Thermohypaesthesia, thermoanaesthesia, thermohyperaesthesia o Pain sensation (investigate with sharp object not needle): analgesia, hypalgesia, hyperalgesia o Light touch (investigate with cotton, avoid stroking) tactil hypaesthesia, anaesthesia, hyperaesthesia • Posterior columns o Vibration sensation (use tunning fork – 128Hz) familiarise the patient with testing on the sternum, start with heel, compare with proximal sites (knee, crista iliaca) pallaesthesia o Joint position hold the sides of the digit, and take it through the smallest movements, bathypaesthesia o Graphaesthesia draw a number on the dorsum of the foot o Two-­point discrimination 0.5 cm on finger tips, 2 cm on feet, use paper-­‐clip • Determine thoracic sensory level (spinal cord lesion) • Dissociated sensory loss (central cord lesion, syringomyelia) CSF examination Pressure: 8-­‐12H2Ocm • Blood: o Colour: ♦ Oxyhemoglobin: red ♦ Bilirubin: yellow ♦ Methemoglobin: brown o Tests: o Oxyhemoglobin: bensidin test o Bilirubin: modified Van den Bergh test o Methemoglobin: potassium-­‐cianid test o Spectorphotometry o Serc: oxyhemoglobin peak at 412-­‐414nm o Sold 1: wide plateau (bilirubin) and peak at 412-­‐414nm (oxyhemoglobin) o Sold 2: maximum at 420-­‐460nm (bilirubin), no peak for oxyhemoglobin (bilirubin: 425-­‐430nm>non-­‐hemorrhagic, 450-­‐
460nm> hemorrhagic) o H-­‐curve: maximum at 406-­‐408> methemoglobin • Glucose: o 2.5-­‐4.3mmol/l o two third of the serum glucose (take 2-­‐4 hours to equlibrium) o low CSF glucose: in pleiocytosis (bacterial, fungal meningitis, tbc, sarcoidosis, SAH) • Cells: o Leukocytes  Meningitis purulenta  Abscessus cerebri  Several tousends of leukocytes  Bacteria: Pneumocossus, Meningococcus, Streptococcus, Staphylococcus, Pseudomonas, Hemophilus,  Fungi: Cryptococcus neoformans, Candida (immunodeficiency!!!) o Lymphocytes  Mononuclear cells  Meningitis lymphocytica, meningitis serosa  50-­‐1000 mononuclear cells/ul  Viri:Adenovirus, Arborirus, Cytomegalovirus, Encephalomyelitis Enterovirus, EBV, HSV, LCM, Influensa virus, etc.  Borrellia burddorferi, Leptospirae, Mycobacterium tuberculosis, Nocardia • Proteins: o Protein content lumbar CSF: 0.2-­‐0.4g/l o Protein content cisternal CSF> 0.05-­‐0.1g/l o Bleeding> 1000rbc/ul = 1mg/dl protein increase o Purulent meningitis> CSF protein might be more than several g/l o Viral meningitis> CSF protein rarely higher than 1g/l o Blockade of CSF circulation> CSF protein > 4-­‐5g/l o Albumin  Synthesized in the liver  Penetrate through the BBB  Comes exclusively from the serum  Increased CSF/Se albumin ratio> BBB disturbance o Immune globulins  IgG, IgA, IgM, IgD, IgE  IgG normally 13% of the Se IgG  IgA and IgM are larger, present only in small amount in CSF  Damaged BBB, intratechal synthesis  Normal range of IgG in CSF> 32.3mg/l  Quantitative analysis of immune globulins • Colloid reaction • Radial immundiffusion • Immunnephelometry (used here) • c individual
variables such as CSF flow rate (8,
age of the patient (11, 12), and volume of CSF
ed.
graphical
presentation
of the CSF and serum
in quotient diagrams is designed to benefit the
n (3). The best discrimination
function or forfor the identification
of an intrathecal
synthesis
unoglobulin
is still subject to discussion (13-16),
here is at least consensus (3) that a nonlinear
ach is essential for discrimination
between bloodd and brain-derived
concentrations
of IgG, IgA,
M in CSF. In the surveys the hyperbolic function
illustrated
in Fig. 1, meanwhile shown to be the
logically
and physically correct form (8, 16), has
introduced. This diagram represents an improved
tion
graph (8) routinely
used for CSF data
s in >80 German or other European neurological
for a clinically
relevant pattern recognition
(4,
.
als and Methods
CSF samples distributed
for proficiency testing
taken from patients punctured
for routine CSF
sis in the Neurologic
Clinic, University
of GotAfter the diagnostic
procedures, residual CSF
es were pooled and kept at -30#{176}C.
Pools of CSF
es and serum samples from patients were cleared
ation
and stabilized by adding 0.1 g/L thimeroodium salt; Sigma, Deisenhofen, Germany).
pairs of CSF and serum samples (0.7 mL each)
uantitative
analysis for total protein, albumin,
IgA, and 1gM were distributed,
with a form for
CSF/serum pair. This data form contained the age
ctitious patient and blank diagrams (see Fig. 1).
Fig. 1. CSF/serum quotient diagrams with hyperbolic functions for
the ratio between
O, #{176}I9M’ and 0Jb
d CSF, which contains
a polyclonal mixture
of
The
upper
discrimination
line
(heaviest curve) differentiates between a bloodcannot be used for qualitative
detection of oligoderived and an additionally brain-derived csF IgG, IgA, or 1gM fraction with
bands. In most surveys the CSF samples for
the following areas (marked on the gG diagram): (1) normal range; (2) pure
blood-CSF barrier dysfunction without local intrathecal IgG synthesis; (3)
on of oligoclonal bands originated from a single
blood-CSF barrier dysfunction plus an intrathecal IgG synthesis in the central
(e.g., ventricular
CSF from a therapeutic
CSF
nervous system; (4) intrathecal lgG synthesis in the central nervous system
without blood-CSF barrier dysfunction. Values in area 5 are indicative of
ge, performed in the intensive care unit, which is
methodological error (unpaired CSF/serum samples, measurement in antigen
y discarded). In one survey single CSF samples
excess range, etc.). The age-dependent evaluation of the blood-CSF barrier
five different patients, each representing
a simifunction is facilitated by the vertical bars, indicating (left to right): 0b at ages
4 months to 15 years, to 40 years, and to 60 years; for newborn children, see
and pattern, were distributed
to participants.
In
Table 1. Dashed lines mark where 20%. 40%, 60%, and 80% of the measured
er survey, for IEF, diluted serum instead of CSF
immunoglobulin concentration in CSF originate from intrathecal synthesis
(lg,,, intrathecal fraction; for calculation see Materials and Methods), referring
used to simulate a corresponding
monoclonal patto the discrimination line as 0% synthesis. Given the imprecision of the
n CSF and serum, typical for a paraproteinemia
methods, any brain-derivedfractions >10% are regarded as pathologicaL#{149},
points representing the report of a participant in the CSF survey indicating
clonal
pattern).
In any case, for detection of
intrathecal synthesis of IgA and 1gM with a blooci-CSF barrier dysfunction
onal IgG the participants
were sent one pair of
(fictitious age of patient, 5 years).This pattern with a dominance of intrathecal
and serum samples (>100 L) and an evaluation•
1gM synthesis is a frequent observation in neuroborreliosis (19, 21).
that included the method-dependent
IgG concentra Qualitative analysis of immune globulins in CSF and serum to avoid preanalytical faults. • Isoelectric pants. Besides
the individual
data for CSF and serum
focusing values, CSF/serum
quotients
had to be reported, nuProcedure
merically and as points in the quotient diagrams on the
mples plus forms were distributed
by regular mail
supplied forms (Fig. 1). For interpretation
of the reNSTAND,
a nonprofit
agency for EQA of the
sults, the following comments were proposed: normal
y of Laboratory Medicine. This EQA organizer is
CSF;
blood-CSF barrier dysfunction;
inflammatory
process; and intrathecal
synthesis of IgG, IgA, and (or)
lled by the Bundes#{228}rztekammer (Federal Medi-
•
•
Immunoblott Compare Se and CSF