...regarding why, once past the BBB, the damage varies from region to region and between individuals. (That "weighty tome" has some interesting stuff in it, guys. )

For example-
1: J Neurosci. 2000 Aug 15;20(16):6309-16.

Regional difference in susceptibility to lipopolysaccharide-induced
neurotoxicity in the rat brain: role of microglia.

Kim WG, Mohney RP, Wilson B, Jeohn GH, Liu B, Hong JS.

Neuropharmacology Section, Laboratory of Pharmacology and Chemistry, National
Institute of Environmental Health Sciences, Research Triangle Park, North
Carolina 27709, USA.

Inflammation in the brain has been increasingly associated with the development
of a number of neurological diseases. The hallmark of neuroinflammation is the
activation of microglia, the resident brain immune cells. Injection of bacterial
endotoxin lipopolysaccharide (LPS) into the hippocampus, cortex, or substantia
nigra of adult rats produced neurodegeneration only in the substantia nigra.
Although LPS appeared to impact upon mesencephalic neurons in general, an
extensive loss of dopaminergic neurons was observed. Analysis of the abundance
of microglia revealed that the substantia nigra had the highest density of
microglia. When mixed neuron-glia cultures derived from the rat hippocampus,
cortex, or mesencephalon were treated with LPS, mesencephalic cultures became
sensitive to LPS at a concentration as low as 10 ng/ml and responded in a
dose-dependent manner with the production of inflammatory factors and a loss of
dopaminergic and other neurons. In contrast, hippocampal or cortical cultures
remained insensitive to LPS treatment at concentrations as high as 10 microg/ml.
Consistent with in vivo observations, mesencephalic cultures had fourfold to
eightfold more microglia than cultures from other regions. The positive
correlation between abundance of microglia and sensitivity to LPS-induced
neurotoxicity was further supported by the observation that supplementation with
enriched microglia derived from mesencephalon or cortex rendered LPS-insensitive
cortical neuron-glia cultures sensitive to LPS-induced neurotoxicity. These data
indicate that the region-specific differential susceptibility of neurons to LPS
is attributable to differences in the number of microglia present within the
system and may reflect levels of inflammation-related factors produced by these
cells.

PMID: 10934283 [PubMed - indexed for MEDLINE]

As for why the variance between individuals (the essential "why doesn't everyone get it?" test:

1: Neuroscience. 2004;124(3):619-28.

Combined toxicity of prenatal bacterial endotoxin exposure and postnatal
6-hydroxydopamine in the adult rat midbrain.

Ling ZD, Chang Q, Lipton JW, Tong CW, Landers TM, Carvey PM.

Department of Pharmacology, 1735 West Harrison Street, Room 410, Rush University
Medical Center, Chicago, IL 60612, USA. zling@rush.edu

We previously reported that injection of the Gram (-) bacteriotoxin,
lipopolysaccharide (LPS), into gravid females at embryonic day 10.5 led to the
birth of animals with fewer than normal dopamine (DA) neurons when assessed at
postnatal days (P) 10 and 21. To determine if these changes continued into
adulthood, we have now assessed animals at P120. As part of the previous
studies, we also observed that the pro-inflammatory cytokine tumor necrosis
factor alpha (TNFalpha) was elevated in the striatum, suggesting that these
animals would be more susceptible to subsequent DA neurotoxin exposure. In order
to test this hypothesis, we injected (at P99) 6-hydroxydopamine (6OHDA) or
saline into animals exposed to LPS or saline prenatally. The results showed that
animals exposed to prenatal LPS or postnatal 6OHDA alone had 33% and 46%,
respectively, fewer DA neurons than controls, while the two toxins combined
produced a less than additive 62% loss. Alterations in striatal DA were similar
to, and significantly correlated with (r(2)=0.833) the DA cell losses. Prenatal
LPS produced a 31% increase in striatal TNFalpha, and combined exposure with
6OHDA led to an 82% increase. We conclude that prenatal exposure to LPS produces
a long-lived THir cell loss that is accompanied by an inflammatory state that
leads to further DA neuron loss following subsequent neurotoxin exposure. The
results suggest that individuals exposed to LPS prenatally, as might occur had
their mother had bacterial vaginosis, would be at increased risk for Parkinson's
disease.

PMID: 14980732 [PubMed - indexed for MEDLINE]

And finally-

1: In Vitro Cell Dev Biol. 1991 Feb;27A(2):113-20.

Blood-brain barrier alterations in bacterial meningitis: development of an in
vitro model and observations on the effects of lipopolysaccharide.

Tunkel AR, Rosser SW, Hansen EJ, Scheld WM.

Department of Internal Medicine, University of Virginia School of Medicine,
Charlottesville.

To further examine the effects of purified Haemophilus influenzae type b
lipopolysaccharide (LPS) on blood-brain barrier permeability, we have developed
an in vitro model of the BBB. Microvascular endothelial cells were isolated from
rat cerebral cortices by enzymatic digestion, dextran centrifugation, and
separation on percoll gradients. The cells were determined to be endothelial in
origin by positive fluorescent staining for Factor VIII-related antigen and the
ability to take up acetylated low density lipoproteins, and their cerebral
origin by the formation of junctional complexes in vitro. Cells were seeded onto
semipermeable polycarbonate filters and permeability assessed by measuring
traversal of radioactive albumin across the monolayer. Treatment of the cells
with LPS at concentrations of 1.0 microgram/ml and 0.1 microgram/ml for 4 h led
to statistically significant increases in albumin permeability of 4.6% (P =
0.001) and 5.6% (P less than 0.001), respectively, without evidence of cell
death as assessed by release of lactate dehydrogenase into the media. These
results indicate that LPS significantly increases albumin permeability across a
monolayer of cerebral microvascular endothelial cells in the absence of host
inflammatory cells. Future studies on the effects of LPS on intracellular
regulation will determine the mechanisms responsible for these alterations.

PMID: 1826902 [PubMed - indexed for MEDLINE]

For those that don't want to wade through the verbage:

1- The bacterial toxin LPS (it's everywhere by the way) can open the BBB;
2- Once inside it makes your microglial defenders go berserk and attack your own tissues;
3- with the help of the excess dopamine we are flooding our brains with?

oooooo!