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FORSKNINGS-PRESENTATION

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Studies of microphysiology of the human motor unit
Erik Stålberg, professor emeritus Collaborators
in the lab Arne Sandberg, Anna Rostedt, Stefan
Stålberg, Lars Karlsson, Björn Hammarberg, Tomas
Winkler
Physiology-pathology
Technical developments
Analysis of EMG signals
Neuromuscular transmission
studies of MG for diagnosis and monitoring
transmission in conditions of reinnervation,
pre- or postsynaptic defects? electrical
stimulation for detailed physiological
measurements.
New recording techniques SFEMG Macro
EMG scanning EMG, New parameters
jiggle size index. Decomposition EM
G Individual MUPs
Motor unit size
normal size variations changes with
pathology in myopathies and neurogenic
conditions dynamic changes in the motor unit
over time in neurogenic conditions (ALS,
polio) Is the development of fatigue in
neurogenic conditions caused by central or
peripheral factors? Is the pathophysiology
underlying the post-polio syndrome also
occurring in other degenerative disorders?
Simulations
EMG simulator SFEMG, Concentric EMG and Macro
EMG can be simulated. Nerve simulator A
motor nerve is simulated.
Studies of single cells in central nervous system
H-reflex and flexion reflexes on single cell
level Cortical stimulation with SFEMG
recordings
Peripheral nerve
Phenomena related to electrical stimulation
Excitability changes (A-waves,
neuromyotonia, el stim)
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Research projects - The Epilepsy Group - UUH
Roland Flink, MD, PhD Collaborators Eva Kumlien,
Elisabeth Ronne-Engstöm
Epileptogenesis
PET studies of focal epilepsy

To increase our knowledge about the different
factors involved in epileptogenesis and the
triggering of epileptic seizures. Laser doppler
recordings together with subdural electrode EEG
recordings have shown changes in the regional
cerebral blood flow prior to seizure activity.
Intracranial micro dialysis is used to analyse
extracellular concetrations of amino acids during
seizures. Experimental studies are performed with
our animal model of focal epilepsy.
Different ligands are used to characterise the
epileptogenic zone in focal epilepsy.
Deoxyglucose shows the metabolism, which is often
decreased in the epileptogenic zone. Deprenyl
binds to the enzyme MAO-B which is mainly located
in the glial cells in the CNS, thus labelling
gliosis. Ketamine will label the NMDA receptors
indicating a possible up regulation in increased
excitatory activity in the brain.
Intracranial laserdoppler recording of regional
blood flow


18Fluoro-deoxy-glucose (FDG)
11C-Ketamine
Intracranial microdialysis
Hypometabolism in right temporal lobe
11C-deuterium-Deprenyl
Focal epilepsy model using ferrous chloride
Increased ketamine binding in left temporal lobe,
binds to NMDA receptor
Increased deprenyl binding in right temporal
lobe, binds to MAO-B enzyme in glial cells
EEG-source localisation

Localise epileptogenic zone from surface EEG
recordings and source analysis with different
dipole algorithms. A realistic three shell head
model with individual conductivity is used and
the dipole location is superimposed on the 3D MRI
reconstruction.
Realistic headmodel
Multimodal imaging
Three shell head model with individual
conductivity
Patient with complex partial seizures
originating from the right frontal lobe
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Microneurography
Karl-Erik Hagbarth, Professor emeritus Main local
collaborators Åke Wallbo, Gunnar Wallin, Erik
Torebjörk, Rolf Hallin, Roland Schmidt, Jan
Fagius, Magnus Nordin and Urban Wallin.
Muscle spindle functions
Exteroceptive functions
Recordings from human muscle spindle afferents
combined with EMG recordings during voluntary
muscle contractions support the
servo-assistance theory. This theory implies
that when a muscle contracts part of the
excitatory drive on the alpha motorneurones is
normally mediated the indirect way via the
fusimotor - motor spindle loop. Other
microneurographic studies indicate that the
hyperrereflexias in spasticity and rigidity are
not primarily due to muscle spindle
hypersensitivity but to increased central
responsiveness to essentially normal spindle
inputs.
Microneurography from human skin nerves combined
with the technique of intraneural
microstimulation has made it possible to analyse
the specific types of sensations aroused by
neural impulse messages signalled by various
types A- and C-fibre sensory units. Studies of
this type have been made both in healthy subjects
and in patients with different types
paraestesias, hyperalgesias and neurogenic pain.
Two types of C-nociceptors have been identified
polymodal units and mechanoinsensitive units
activated by algogenic substances. A special type
of C-units are histamine responsive and give rise
not to pain but to itch sensations. The technique
allows differentiation between chronic pain
syndromes due to peripheral nicoceptor
hyperexitability and to increased responsiveness
of central sensory neurones.

Sympathetic functions
Besides the traffic of impulses in various types
of afferent nerve fibres also the impulse traffic
in post ganglionic sympathetic C-fibres can be
recorded with the microneurography technique. It
has been shown that the sympathetic activity in
muscle nerve fascicles consists of
vasoconstrictor impulses which under baroreflex
control serve to guard against sudden falls in
diastolic blood pressure. In contrast, the
sympathetic activity in skin nerve fascicles
consists of a mixture of vasomotor and sudomotor
impulses which, besides giving rise to
cold-sweatreponses to various types of arousal
stimuli - also sudserve thermoregulatory
functions. A great number of studies of
sympathetic activity in muscle and skin nerves
have been performed as well in healthy subjects
of various age as in patients with various types
of autonomic disturbances.
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Research Projects - in Clinical Neurophysiology
Karin Edebol Eeg-Olofsson, MD, PhD Collaborators
D.Tshala (Konzo), S. Lundberg (Rolandic
epilepsy), U. Karlbom and A.Österberg
(Gastrointestinal neurophysiology)
Konzo
Rolandic Epilepsy
Konzo is a subacute spastic para/tetraparesis in
central Africa and is related to intake of bitter
cassava. 1998 and 2000 high-tech equipment was
brought from our Department to Kinshasa for
neurophysiological investigations on konzo
subjects and their relatives.
Rolandic epilepsy is a concept used for focal
epilepsies where rolandic spikes are found. In
Uppsala, MRI and neuropsychology have been
performed on children with benign epilepsy with
centrotemporal spikes.
Results MRI overrepresentaton of pathological
changes. Neuropsychology several abnormalities
especially in learning. I.e. benign childhood
epilepsy not always benign. Rolandic epilepsy
heterogeneous.
Results EEG overrepresentation of
abnormalities. (slowing of activity) Neurography
normal EMG small motorunit potentials. MEP
abnormalities. SEP abnormal findings. Muscle
biopsies atrophic changes.
Gastrointestinal neurophysiology

Gastrointestinal neurophysiology implies
disorders of constipation and faecal
incontinence. Different methods may be used for
mapping. In co-operation with the Department of
Surgery, above disorders have been investigated
on large patient materials.
Results Constipation via hook-electrodes
increased paradoxical activation of external anal
sphincter and puborectalis muscle were
found. Incontinence increased distal pudendal
latency and fibre density in the majority of
patients.
Electrical cortical stimulation in konzo
Kabambu, 18year old, with konzo
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Neurophysiological evaluaton of spinal cord
injuries
Tomas Winkler MD, PhD Collaborators Hari
Shanker Sharma MD, Prof. em. Erik Stålberg, Prof.
Fred Nyberg, Prof. Per Alm.
Results
A spinal cord injury is followed by 1. immediate
loss of conduction in spinal cord
tracts (spinal chock), 2. from five min
progressive destruction of grey tissue
(secondary injury), 3. from three hours secondary
injury changes also in white tissue. Which
factors are involved in spinal shock and
secondary injury? Could these factors be
influenced by pharmacological treatment?
Immediately after injury negative response in
rostral recordings is lost and replaced by a
positive injury potential (fig 1, 0 min fig
2a). These animals show five hour after injury
pronounced swelling and histological detoriation
in injured segments (fig 2b).
Treatment before injury with drugs listed below
partly or completely abolished both the spinal
shock and the pathological changes seen five hour
after injury (fig 2) P CPA
serotonin synthes is inhibitor Indomethacin
prostaglandin synthesis is
inhibitor Naloxone opoid
receptor blocker NO synthase antiserum Cimetidine
histamine receptor
blocker Nimodipine Ca
channel blocker Ibuprofen
anti-inflammatoric
(serotonin receptors?) Diazepam
benzodiazepine receptors Topical application
of IGF-1 (insulinlike growth factor) Topical
application of rGH (rat growth hormone) No
effect of following drugs (fig 2) Dexamethasone
anti-inflammatoric
steroid Propranolol
B-receptor blocker Phentolamine
A-receptor blocker Increase of secondary
injury (fig 2) Crypoheptadine
serotonin receptor blocker
Methods
Laminectomy at T10-11 in anesthetized rats,
recording of epidural evoked potentials from T9
and T11 after stimulation of nerves in the right
hindlimb, longitudinal inscision in the right
dorsal horn of T10-11 (i.e. passing tracts not
involved by the primary injury), five hour after
injury measurement of water content and
hist-pathological analysis of injured segments.

Fig.1
Conclusion
Several substances are released immediately
after a spinal cord injury, they are all
essential for the development of secondary
injury. Later blocking of these substances does
not influence the course. Topical application
possible and more effective.
Fig.2